3RD EDITION

Care of the
Critically Ill Surgical Patient
EDITED BY IAN LOFTUS
First published in Great Britain in 1999 by Hodder Arnold
Second edition 2003
This third edition published in 2010 by
Hodder Arnold, an imprint of Hodder Education,
part of Hachette Livre UK, 338 Euston Road, London NW1 3BH

http://www.hodderarnold.com

2010 The Royal College of Surgeons of England

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 CONTENTS

CONTENTS

Chapter Title Page

Foreword to 1st edition VI
Preface VIII
CCrISP course objectives XI
Abbreviations XII
Normal laboratory values XIV
1 Introduction 1
2 Assessment of the critically ill surgical patient 11
3 Airway and tracheostomy management 25
4 Respiratory compromise in the surgical patient 33
5 Arterial blood gases and acidbase balance 51
6 Cardiovascular disorders, diagnosis and management 59
7 Shock and haemorrhage 89
8 Cardiovascular monitoring and support 105
9 Renal failure, prevention and management 121
10 Peri-operative management of the surgical site 137
11 Fluid and electrolyte management 155
12 Sepsis and multiple organ failure 167
13 Nutrition in the surgical patient 183
14 Pain management 197
15 Communication, organisation and leadership in surgical care 213
16 Assessment of surgical risk and peri-operative care 227
Index 240
Success depends
upon attention to
detail
Joseph Lister 1827-1912
 CONTRIBUTORS

CONTRIBUTORS TO THE 3 RD EDITION

Mr Ian Loftus BSc MB ChB MD FRCS Dr Philip Newman FRCA

Consultant Vascular Surgeon and Reader Consultant Anaesthetist, St Georges Hospital,
in Vascular Science, St Georges Hospital, London London
Editor and Critical Care Tutor,
Mr Declan OBrian FRCA
The Royal College of Surgeons of England
Consultant Anaesthetist, Cork University Hospital
Mr Iain Anderson FRCS
Professor Rob Sayers FRCS
Consultant Surgeon, Hope Hospital, Salford
Consultant Vascular Surgeon,
Dr Daniele Bryden FRCA Leicester Royal Infirmary
Consultant Anaesthetist, Northern General Hospital
Mr Mark Taylor PhD FRCS
Mr Francis Calder FRCSEd Consultant General and Hepatobiliary Surgeon,
Consultant Transplant Surgeon, Guys Hospital, Mater Informorum Hospital, Belfast
London
Dr Joseph Cosgrove FRCA
Consultant Anaesthetist, Freeman Hospital,
Newcastle
Dr Sarah Gillis FRCA CONTRIBUTORS TO THE 2 ND EDITION
Consultant Anaesthetist, Whittington Hospital, Mr G L Carlson FRCS
London Dr M Hunter FRCAS
Dr Jonathan Goodall FRCA Dr B Riley FRCA
Consultant in Intensive Care, Hope Hospital, Salford Professor B J Rowlands FRCS
Dr G B Smith FRCA
Mr John Jameson FRCS Professor M M Thompson FRCS
Consultant General Surgeon,
Leicester General Hospital CONTRIBUTORS TO THE 1ST EDITION
Mr Brian Johnson FRCS Dr T N Appleyard
Consultant Vascular Surgeon, Hull Royal Infirmary Professor K CH Fearon
Mr D R Griffin
Mr Keith Jones FRCS
Professor D J Leaper
Consultant Vascular Surgeon, St Georges Hospital,
Dr G Ramsay
London
Mr R C G Russell
Professor J M Ryan
Dr A I K Short
Dr S W Turner
Dr R G Wheatley
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

ACKNOWLEDGEMENTS

Mr Adrian Anthony MB BS FRACS

Consultant Surgeon,
Queen Elizabeth Hospital, Australia
Mr Adam Brownsell
Publisher,
The Royal College of Surgeons of England
Miss Emma Church
Development and QA Coordinator,
The Royal College of Surgeons of England
THIS BOOK IS DEDICATED TO

Mr and Mrs Leon Grant

CARE OF THE CRITICALLY ILL SURGICAL PATIENT

FOREWORD TO 1 ST EDITION

On Saturday 15 April 1989, at a football match

in the English city of Sheffield, an incident
occurred in a tightly packed crowd which resulted
in 96 mainly young people being crushed to
death with many others seriously injured. The
name of the football ground, Hillsborough, has
become embedded in the English language as
being synonymous with a major civilian disaster
associated with needless loss of life. It would be
difficult to see how anything positive could
emerge from such a tragedy but there is a
precedent, admittedly on a much smaller scale.
In 1976, in rural Nebraska, USA, a plane being
piloted by an orthopaedic surgeon crashed. One
of the six occupants was killed instantly and four
were critically injured. The primary care received
by the injured was judged by the doctors at the
admitting hospital, and the orthopaedic surgeon
himself, to be less than ideal. As a result the local
surgeons decided that they should take some
action to establish innovative training courses
to help those unused to managing the seriously
injured to deal with such cases. Thus arose the
now well-recognised and respected Advanced
Trauma Life Support (ATLS ) courses which use
simulation and scene setting to mimic major
injury and to improve the quality and realism
or training.

VI

In 1988 ATLS was introduced into the United
Kingdom by The Royal College of Surgeons of
England and became instantly popular with
all those tasked with the management of the
seriously injured, and there is no doubt that ATLS
techniques were used at Hillsborough and may
well have prevented an even higher death rate.
Although difficult to prove scientifically, there
is virtually universal agreement that ATLS
courses have improved care and contributed to
the lowering of the death rate after road traffic
accidents which has become such a marked
feature of United Kingdom accident statistics
of recent years. ATLS however, deals only with
the early stage of injury and there is undoubtedly
a need for improvement in the management
of that critical period following injury, during
critical surgical illness, or after major surgery
where patients may be in intensive therapy or
high dependency units.
The educational techniques used in ATLS
are equally applicable in critical care training.
Iain Anderson and his colleagues, with the help
of the Education Department at The Royal College
of Surgeons of England and the support of the
Hillsborough Charity, have produced a course
similar in concept to ATLS and using its
techniques, dealing with the management of the
critically ill surgical patient. This book is produced
in a format that will enable the text to be used
either independently or alongside the course.
This innovative approach has the potential for
improving the care of critically ill patients in
the same manner and to the same degree as that
achieved by ATLS .
VII
FOREWORD TO 1ST EDITION
The book deals concisely and clearly with the
whole range of issues associated with the critically
ill, including the management of the psychological
problems which were such an issue after
Hillsborough. The surgical trainees who undergo
this course and read this textbook will have
restored to them the confidence once felt by
all surgical trainees in the management of the
critically ill. This confidence was based on the
famous textbook by the American surgeon Francis
Moore, The Metabolic Care of the Surgical Patient,
a book that is widely accepted as being the
foundation stone of modern intensive care.
I hope those so tragically bereaved at Hillsborough
will regard this book and its accompanying
course as a living addition to the more permanent
memorial in Liverpool to those who died.
Sir Miles Irving
DSc (Hons) MD ChM FRCS FACS (Hon) FMedSci
Emeritus Professor of Surgery,
University of Manchester
Chairman of Newcastle upon Tyne Hospitals
NHS Trust
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

PREFACE

Surgical training has undergone major changes

over the last decade. While hours of duty for
doctors in training have been reduced by
legislation designed to improve patient care, so
clinical exposure has been reduced and traditional
surgical teams fragmented. One could argue that
modern day surgical trainees are under more
pressure than ever before, despite the reduction
in working hours. Trainees often feel disengaged
from their trainers, and their patients, due to shift
working patterns that are disruptive to traditional
training methods. Moreover, because of a lack of
clinical exposure, they often feel unprepared to
deal with emergencies and the care of the critically
ill patient.
The Care of the Critically Ill Surgical Patient
(CCrISP) course remains a valuable adjunct to
traditional ward training and continues to
provide young surgeons with the structure and
confidence they require to safely and effectively
care for their patients on the ward and in theatre.
This third edition of the course, originally
launched by Iain Anderson and colleagues in
1996, remains true to the original aims to take
responsibility for critically ill surgical patients,
to predict and prevent problems that patients
might encounter while in hospital, to function
well within the surgical team and communicate
effectively with colleagues from other disciplines.

VIII
 PREFACE

The CCrISP course was originally established by The CCrISP algorithm for simultaneous assessment
a multidisciplinary team of surgeons and and resuscitation has become the benchmark for
anaesthetists with a grant from the Hillsborough the management of surgical patients and is used
football stadium disaster. Many of the original by even the most senior, experienced surgeons on
group continue to instruct on the CCrISP course a daily basis.
and some have been involved in this latest As with previous editions, this review is based
iteration of the material and manual. The majority on the opinions of a multidisciplinary steering
of surgical trainees in the UK take the course, group that has worked tirelessly to ensure that
available in over 60 centres, and it is compulsory it represents the needs of current surgical
in Australasia. More recently, the START trainees. I hope that you will find it instructive
(Systematic Training in Acute Illness Recognition and beneficial to the care you provide to
and Treatment) Surgery course has adopted the your patients.
CCrISP principles successfully for the training of
foundation year doctors. A CCrISP Instructor
course also runs at The Royal College of Surgeons
of England to prepare senior surgeons, who have
all taken the CCrISP course during their training,
for providing the course nationwide. This Ian Loftus
continuum of surgical critical care training has
been supported generously for many years by
Jane and Leon Grant, to whom this third edition
is dedicated.
The new edition of the course continues to
reinforce the clinical application of the theory
base provided in this manual. The manual has
been updated significantly, with some chapters
removed entirely, replaced with new chapters felt
to be more relevant to current surgical trainees.
The principles remain the same to encourage the
development of practical skills, improved patient
management and the development of interpersonal
skills required to work effectively and confidently
within a surgical team. The need to master these
skills early in training has never been more
pressing, given the changes to working patterns
and demands on time.

IX
A stitch in time
saves nineTraditional
 COURSE OBJECTIVES

CCrISP COURSE OBJECTIVES

Develop the theoretical basis and practical Be aware of the support facilities available
skills necessary to manage the critically ill and interact with nursing staff, other surgeons
surgical patient and intensivists/anaesthetists, being aware, in
Be able to assess critically ill patients accurately particular, of the surgeons role in the delivery
and appreciate the value of a system of of multidisciplinary care to the critically ill
assessment for the critically ill Understand the requirements of the patient
Understand the subtlety and variety of and his or her relatives during critical illness
presentation of critical illness and the methods and be able to inform and support both
available for improving detection appropriately.
Understand the importance of a plan of action
in order to achieve clinical progress, accurate
diagnosis and early definitive treatment. Be able
to formulate a plan of action and involve
appropriate assistance in a timely manner
Appreciate that complications tend to occur
in a cascade and realise that prevention of
complications is fundamental to successful
outcome

XI
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

ABBREVIATIONS

ABG arterial blood gas DPL diagnostic peritoneal lavage

ACE angiotensin-converting enzyme DVT deep vein thrombosis
ACS acute compartment syndrome
ADH antidiuretic hormone ECF extracellular fluid
A&E accident and emergency ECG electrocardiogram
AF atrial fibrillation ECLS extracorporeal life support
AKIN acute kidney injury network EEG electroencephalogram
AP anteroposterior EIA epidural infusion analgesia
ARDS acute respiratory distress syndrome ENT ear, nose and throat
ASB assisted spontaneous breathing ERCP endoscopic retrograde
ATLS Advanced Trauma Life Support cholangiopancreatography
AV atrioventricular
FAST focused abdominal sonography
BAL bronchial alveolar lavage in trauma
BBB bundle branch block FBC full blood count
BCAA branched-chain amino acid FEV1 forced expiratory volume in 1 s
BE base excess FRC functional residual capacity
BLS basic life support FTc corrected flow time
BMI body mass index
BSA body surface area GABA gamma-aminobutyric acid
GCS Glasgow coma scale
CCF congestive cardiac failure GI gastrointestinal
CCrISP Care of the Critically Ill Surgical Patient
CI cardiac index HDU high dependency unit
CNS central nervous system HIV human immunodeficiency virus
COAD chronic obstructive airways disease 5-HT 5-hydroxytrptamine (serotonin)
COX-2 cyclo-oxygenase 2
CPAP continuous positive airway pressure IAP intra-abdominal pressure
CPP cerebral perfusion pressure ICU intensive care unit
CPR cardiopulmonary resuscitation ICP intracranial pressure
CRF chronic renal failure IgE immunoglobulin E
CSM carotid sinus massage IHD ischaemic heart disease
CT computed tomography IVNAA in vivo neuron activation analysis
CTZ chemoreceptor trigger zone IVU intravenous urogram
CVP central venous pressure
CVS cardiovascular system JVP jugular venous pressure
CXR chest X-ray

XII
 ABBREVIATIONS

LAP left atrial pressure RRT renal replacement therapy

LFT liver function test
LVEDP left ventricular end diastolic pressure SIMV synchronised intermittent
LVEDV left ventricular end diastolic volume mandatory ventilation
LVF left ventricular failure SIRS systemic inflammatory response
syndrome
MAP mean arterial pressure SVC superior vena cava
MEWS modified early warning score SVR systemic vascular resistance
MI myocardial infarction SVT supraventricular tachycardia
MOF multiple organ failure
MRI magnetic resonance imaging TNF tumour necrosis factor
MRSA methicillin-resistant Staphyloccus aureus TOD trans-oesophageal Doppler

NCA nurse-controlled analgesia VF ventriculation fibrillation

NICE National Institute for VT ventricular tachycardia
Health and Clinical Excellence
NIV non-invasive ventilation WPW Wolff-Parkinson-White syndrome
NSAID non-steroidal anti-inflammatory drug

OSA obstructive sleep apnoea

PA postero-anterior
PAOP pulmonary artery occlusion pressure
PAP pulmonary artery pressure
PCA patient-controlled analgesia
PCIRV pressure-controlled inverse
ratio ventilation
PCV pressure-controlled ventilation
PCWP pulmonary capillary wedge pressure
PE pulmonary embolism
PEEP positive end expiratory pressure
PEM protein-energy malnutrition
PiCCO pulse contour cardiac output with
dicator dilution
PSV pressure-support ventilation
PTC percutaneous trans-hepatic cholangiography
PTSD post-traumatic stress disorder

XIII
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

NORMAL LABORATORY VALUES

Measurement Normal range

Sodium 135145 mmol/l
Potassium 3.55.0 mmol/l
Urea 3.17.9 mmol/l
Creatinine 75155 mol/l
Total protein 5878 g/l
Albumin 3450 g/l
Calcium 2.122.60 mmol/l
Phosphate (PO43-) 0.80 1.44 mmol/l
Bilirubin 019 mol/l
Alkaline phosphatase 35120 units/l
ALT 045 units/l
Creatine kinase Male: 38174 units/L | Female: 96140 units/L
Haemoglobin 13.018.0 g/l
Platelets 150450 x 109/l
White cell count 4.011.0 x 109/l
Prothrombin time 11.013.0 s
APTT 2439 s
Fibrinogen 1.54.0 g/l
pH 7.357.45
PaCO2 4.55.5 kPa (34-42 mmHg)
PaO2 11.014.0 kPa (83105 mmHg)
HCO3- 24 28 mmol/l
Base excess -2 to +2 mmol/l
Lactate 0.4 1.7 mmol/l

XIV
1
Introduction

1
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Looking after critically ill surgical patients
successfully is a major and, at times, stressful part
of the surgeons life. Surgical practice is dynamic
and as changes to hospital practice occur, they
may help or hinder other aspects of the delivery
of care. Some of the current factors are shown in
Table 1.1.
TABLE 1.1
RISK AND STRESS FACTORS
IN SURGICAL CRITICAL CARE
Ageing population
Concomitant disease processes
Complexity of surgery
Higher standards of monitoring
Greater number of postoperative
interventions and therapies
Expectations by patients, relatives
and staff
Shortage of permanent and experienced
nurses
Shortened duty hours for junior surgeons
and different on-call arrangements
Many surgical patients are old, sick, have
undergone major surgery or have had emergency
admission. With modern duty arrangements, you
will often be responsible for this type of patient
from other surgical teams and you may well be on
duty with junior and senior staff with whom you
only work occasionally. Consequently, the duty
surgeon will be faced frequently with critically ill
surgical patients with whom they are not familiar.
The establishment of high dependency units
(HDUs) has been an undoubted advance but not
all unwell patients can be cared for there and, in
any event, patient care in HDU often remains the
2
responsibility of the surgical team. Furthermore,
to the unfamiliar, the HDU can be a daunting
place. The CCrISP programme provides practical
training to support the junior doctor who is faced
with managing unwell surgical patients today. In
particular, it provides a simple, safe and accepted
approach with which you can begin to assess and
manage every patient you encounter, no matter
how complex.
The capacity of surgical patients to withstand
surgery and any complications depends on
their age, underlying disease process and any
co-existing illnesses. Once surgical patients
develop multiple organ failure (and hence
require intensive care unit [ICU] support),
overall mortality can be around 50%. It is clear,
therefore, that detecting and treating problems
before this stage is reached is much the preferable
course of action. Unfortunately, critical surgical
illness can often be detected easily only once
a relatively advanced stage has been reached.
The challenge for all surgeons who deal with
patients who may become critically ill is to
develop a system of practice which will allow
the identification and correction of complications
at the earliest stage. Improvements can be
achieved through three mechanisms as summarised
in Table 1.2.
TABLE 1.2
COMPLEMENTARY APPROACHES
TO CRITICAL CARE
Prediction: identifying an at-risk population
Prevention
Prompt identification and early adequate
treatment

These are complementary and will apply in
differing proportions to different patient groups.
These strategies are at least as important
components of surgical critical care as the heroic,
but often unsuccessful, rescue of the patient who
has reached a state of extremis.
AIM OF TRAINING
IN SURGICAL CRITICAL CARE
Critical illness begins, is detectable and treatable
long before a patient arrives in an ICU with
multiple organ failure, and the aim of this
manual and its related course, the CCrISP course
of The Royal College of Surgeons of England,
is to equip you to predict, prevent and treat these
patients accordingly. Likewise, it will be difficult
to offer best care to emergency cases or to unfit
patients upon whom you conduct major surgery
without the necessary management skills for
ward and HDU practice. Surgical training has
traditionally focused on pathology and operative
surgical treatment; however, with the advances
in critical care techniques and changes in
patient demographics, more structured teaching
in non-operative management of critically ill
patients is essential.
AIMS OF THE CCrISP COURSE
Improve practical management of critically
ill surgical patients
clinical method
practical skills
communication and organisational skills
focused knowledge.
3
CHAPTER 1 | INTRODUCTION
Too many deaths or unplanned admissions to
ICU occur because appropriate, thoughtful and
early action was not taken. Studies show that
3040% of patients admitted to ICU received
sub-optimal care on the ward at some stage.
Together with the CCrISP course, this book aims
to make you think about the ill or potentially ill
patient. It will help you identify the patient who
may become ill and take the necessary steps to
prevent that patient developing complications;
to deal with any emergency arising on the ward;
to assess and respond to the immediate problem;
and to initiate treatment while awaiting specialist
help. Following immediate management, you will
learn the importance of identifying and correcting
the underlying cause. Many adverse episodes can
be terminated by the immediate provision of
simple support (e.g. oxygen, fluids) and by the
early attainment of a diagnosis so early definitive
treatment can be instituted (e.g. antibiotics,
provision of usual cardiac medications, drainage
of an abscess).
PRACTICE POINT
Prompt, simple actions save lives and
prevent complications.
Avoidable problems occur because these simple
manoeuvres are not taken or, more commonly,
their effectiveness and adequacy is not checked
and further effective steps not taken. For example,
failure to institute and ensure effective support
for an elderly patient with retained pulmonary
secretions on a Saturday may result in established
pneumonia by Monday morning. Survival may be
threatened and length of stay will certainly be
prolonged (Case Scenario 1.1).
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 1.1

A 68-year-old man, a smoker with mild chronic airways disease, underwent a laparotomy for a
perforated duodenal ulcer on Monday night. An epidural was placed but was removed on day 4
(Friday). He received chest physiotherapy during the week but no specific request was made for
weekend treatment. His team was not on call and, as he seemed to be progressing, no formal
handover was made. On Saturday afternoon, he was noted to be in pain and to have a tachypnoea.
The foundation year doctor was called but was busy and did not see him until 9 a.m. by which time
he was pyrexial. A course of ciprofloxacin was prescribed (although none would be available from
the pharmacy until 9 a.m.). He was reviewed at the end of the on-call ward round, late Sunday
morning, and found to have deteriorated considerably, with pyrexia, dyspnoea and bronchial breathing.
He was started on monitored oxygen, nebulisers and urgent chest physiotherapy was arranged,
following review of his requirements for analgesia. He took 10 days to get over the pneumonia and
his hospital stay was prolonged by about 2 weeks.

LEARNING POINTS
the best critical care is simple and preventive late, heroic interventions are less successful
prompt, simple actions save lives and prevent complications
make, use and update action plans
success depends on attention to detail.

Achieving simple interventions, such as the
oxygen, nebulisers and physiotherapy in the case
above, requires the same combination of skills as
more complex or dramatic episodes in surgical
critical care. These include clinical examination,
judicious investigation, formulation of a plan
of action, institution thereof (including the
necessary communication with colleagues and
practical techniques), and re-evaluation of the
patient with, if necessary, the ability to invoke
greater degrees of support at the right time.
These skills, together with relevant practical
procedures and the related base knowledge,
will be taught and assessed in simulated clinical
situations during the CCrISP course, the emphasis
throughout being on practical management of
common problems. However, there is no reason
why you cannot adopt a systematic approach to
your own practice directly.
PRACTICE POINT
Re-assess!
Has your intervention been effective?
Further prompt and simple actions may
be necessary.

4

WHAT THIS MANUAL IS NOT
Neither this manual nor the CCrISP course will
teach you to become a specialist in intensive care!
Instead, the main thrust is about prevention of
further deterioration through accurate and
prompt ASSESSMENT and TREATMENT to avoid
complications on the ward and in HDU. However,
there does exist a considerable overlap between
the practical skills and approaches to care seen on
ICU and in the surgical HDU and junior surgeons
benefit greatly from a period spent working on
ICU. Surgeons must be aware of the nature and
principles of intensive care, the support available
there and the time when such support should be
sought. They must also be aware of the limitations
of ICU and the nature of support which the
surgical team must provide to the ICU team when
their patients are being treated on ICU. During
your training, you will need to develop an
appreciation of the surgical needs of patients in
ICU, the difficulties of assessment there and the
impact of ICU care on your patients and their
disease processes. Following discharge from ICU,
a further range of skills is necessary to ensure
that the patient does not fall into the trap of
early deterioration and re-admission to ICU.
These topics will be dealt with and will contribute
towards making you a better practitioner of
surgical critical care.
This manual takes a practical, management
orientated approach to critical care. It is not
designed to be a comprehensive text of surgical
critical care and you may wish to supplement
your reading from such a text, particularly for
membership examinations.
5
CHAPTER 1 | INTRODUCTION
CONTINUUM OF CARE
In fact, there is a continuum of care from the
ICU through HDU and ward to the community and
each provides different attributes of importance
to successful surgical care. Compared with surgical
wards, the HDU is an area of enhanced nurse to
patient ratio (1:2), with appropriate monitoring
(arterial, CVP, pulse oximetry, heart rate) equipment
and accumulated nursing expertise in both critical
illness and specialist surgical care. Patients are
usually within 2472 hours of operation and either
at high risk of complications or have developed a
complication or impairment of vital organ function
on account of their illness, surgery or co-existing
medical disease. Some HDUs will manage patients
with single organ failure but the main aim is to
detect and prevent further deterioration.
By way of contrast, ICU offers more intensive
nursing ratios, monitoring and support, and care
is usually directed by intensive care medical staff
in collaboration with the patients surgical team.
Here, failed organ systems can be supported by
complex interventions (e.g. ventilation, high dose
or multiple inotrope therapy, haemofiltration or
dialysis). ICU staff may be less experienced than
their HDU counterparts in the surgical aspects
of management of patients following complex
procedures.
Although the precise profile of patients in different
critical care units will vary between hospitals,
you should note that many patients will require
surgical and intensive care type input whichever
type of bed they are in surgeons have a role to
play in the care of patients on ICU and ICU staff
often help manage patients on the ward. The
proportion of care needed from each team will
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

vary with time and with the patients immediate THE PATIENTS TO BE CONSIDERED
needs (Fig. 1.1). HDU occupies a middle ground
in terms of the balance between management of
surgical problems and the management of
systemic or multi-organ problems.
Increasing surgical input
Surgical input
Situations in which patients are considered
at risk or that may increase risk are summarised
in Table 1.3. In caring for critically ill surgical
patients, three categories of patients can be
discerned:
the routine pre-operative patient
the emergency admission
the ward patient.

TABLE 1.3
ICU input
Patients at risk
Emergencies
ICU HDU Surgical ward Elderly
Co-existing disease processes
Increasing ICU input Non-progressing patient
Severity of acute illness or magnitude
Figure 1.1 Changing requirements for critical support in of operation
surgical patients. Massive transfusion
Re-bleeding
Failure/delay to diagnose and treat
Special surgical units (e.g. transplant units) offer
underlying problem
varying combinations of facilities. Assessing
Already developed another complication
and managing patients there will require specialist
Established shock state
knowledge and techniques but most of the
immediate management relies on the same basic Practices that increase risk
principles. Indeed, many complex problems in Incomplete or infrequent assessment
critical care can be broken down, assessed and Failure to act on abnormal findings
treated in a similar manner. Failure to ensure that interventions have
been successful
Failure of continuity of care
(poor communication)
Failure of nursing support (insufficient
numbers or expertise) wrong ward

6
 CHAPTER 1 | INTRODUCTION

Pre-operative patient emergency major surgery are inherently

Patients on steroids for severe chronic airways
disease, for example, present obvious risks.
Here, a balance must be struck between necessity
of operation and the individual risks. Careful
specialist and anaesthetic assessment will be
needed, if not already obtained, and plans will
need to be made for postoperative care. Less
obvious problems may act synergistically but a
similar approach can minimise their effect (see
Case Scenario 1.2).
The emergency admission
Emergency admissions present with a wide variety
of underlying diseases and an equal spectrum
of co-morbid conditions ranging from the
unrecognised (e.g. occult ischaemic heart disease)
to the obvious (e.g. anticoagulation), which
complicates matters. Many patients undergoing
unstable and easy prey to further complications.
Preventing these begins by achieving prompt
and effective resuscitation and surgery no easy
matter in an elderly group presenting out of normal
working hours. Anaesthesia removes vascular
tone and can cause catastrophic hypotension in
the hypovolaemic patient. It is obvious that you
cannot do the laparotomy on the patient with
peritonitis until he or she is resuscitated but
a patient with a fractured neck of femur also
requires careful resuscitation. On the other hand,
you must identify the bleeding patients who
need simultaneous surgery and resuscitation.
Co-ordinating appropriate care following surgery,
especially out of routine hours, can tax your
organisational and communication skills. Clear
guidelines must be given to nursing staff and
regular medical review undertaken.

CASE SCENARIO 1.2

Take, for example, the patient for inguinal hernia repair who appears fit but who has left BBBV,
a smokers cough, mild alcoholic liver disease and prostatism. After operation, a predictable chain of
minor events may ultimately prove fatal: simple hernia repair leads to urinary retention; subsequent
urine infection contributes to a confusional state; failure of expectoration causes atelectasis, then a
chest infection; underlying ischaemic heart disease cannot cope with hypoxia. The patient suddenly
arrests on day 3 on the short stay ward.
Much of this could have been and should have been predicted. A downward spiral starts with the
requirement for a urinary catheter. The significant premorbid conditions contribute to the rapid
and relentless deterioration which ultimately leads to the patients demise.

LEARNING POINT
It is crucial to predict and prevent problems, consider the pros and cons of surgery in each
individual case, and optimise patients appropriately if surgery is essential.

7
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
The Ward Patient
The routine ward round
On business ward rounds, you will review all
your patients; in fact, this is probably the most
important way in which you practise good critical
care. By conducting a logical and thorough round,
you can prevent or identify many problems and
get them corrected before they cause significant
upset. The system of assessment and formulation
of management plans described in the next chapter
applies to these patients every bit as much as to
those who are obviously unwell.
The ward patient with complications
Patients who develop obvious complications
present similar challenges to the emergency
admissions the major pitfall being a failure
to take further prompt action when initial
interventions are not sufficiently successful.
More difficult are patients who fail to progress.
Here, there is usually an underlying problem
eluding detection. These patients are often
elderly; the recognition of subtle signs can lead
to appropriate action preventing major problems
arising as indicated in Case Scenario 1.2 above.
8
METHOD OF APPROACH
Basic surgical trainees are essentially data
gatherers they pass information to seniors.
As you progress in seniority, your role changes.
You will shortly become a senior trainee, where
you will be much more of a decision maker. You
will make critical decisions constantly on ward
rounds or about emergencies which will have
a direct bearing on patient outcome. Of course,
you will have senior colleagues with whom to
discuss things; nevertheless, there is a marked
change in role and responsibility at this stage.
Using the skills and approaches described in this
manual and on the CCrISP course will help you
appreciate some of the changes you need to
develop. These will aid the change, when it comes,
to be less stressful and more successful for all.
All clinicians find the management of emergencies
stressful at times and this is usually made worse
by a lack of information (about the patient, their
diseases or recent events), disorganisation and
initial lack of appreciation of the severity of the
situation. You will, by now, have experienced
episodes in your own practice of critical illness
that were not managed as well as they might have
been it is useful at this stage to reflect on the
reasons why those sub-optimal events occurred.
The aim now is to build on your present
knowledge and experience to train you to
think, to be in command of any situation by
rapidly assessing the situation and the patient,
responding to the immediate problem and
initiating treatment. Certain simple immediate
thoughts can help set your assessment off on
the right foot (Table 1.4).
 CHAPTER 1 | INTRODUCTION

SUMMARY
TABLE 1.4 Preventing deterioration is more effective than
attempting salvage at a later stage
THINKING ON THE RUN Surgical critical care includes prediction and
Think early when the phone call comes prevention of problems as well as investigation
instructions to caller and intervention in the acutely unwell
what do I know about ...? There is a continuum in surgical critical care
what will I do when I arrive? extending from the ward level (prediction,
Think basics when I arrive prevention) to HDU and upwards to integrate
check and secure the ABCs with intensive care
what system fails? Simple logical thought and actions will often
what observations are available? be effective.
what observations can I make quickly?
Think simply
how quickly must I act?
do I have a diagnosis?
how will I get that diagnosis safely?
what help do I need?
THINK THEN ACT

The CCrISP programme will emphasise certain

quite basic clinical and scientific concepts: those
that clinicians experienced in this field employ
in front-line practice. Above all, it will help you
think straight when you are under pressure in
the clinical arena. It will provide you with
mechanisms that will facilitate successful care,
the most important of which is a systematic
means to assess a critically ill surgical patient.
Until now, you will have approached problems
by taking a detailed history and then examining
the patient. However, critically ill patients
require a system that lets you identify and treat
problems rapidly, according to priority and as
you further assess the patient. This approach
is detailed in the next chapter.

9
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

10
2
Assessment of
the critically ill
surgical patient

11
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

is present. If you fail to diagnose and treat that

OBJECTIVES problem until it has produced a major deterioration
in the patients condition, then the patients
This chapter will help you to:
likelihood of survival is dramatically reduced.
assess and manage critically ill patients
The approach to the assessment of the sick
systematically
surgical patient should be systematic to ensure
recognise the critically ill patient who
that life-threatening or potentially life-threatening
must undergo simultaneous examination
conditions and important aspects of care are not
and resuscitation when first seen
overlooked. Employing a system regularly ensures
recognise that examination and resuscitation
that you will use it when you are under pressure.
must be performed in a systematic manner
The CCrISP system of assessment is shown in
treating life-threatening problems in the
Fig. 2.1. It is the system that many experienced
order of their threat to life
doctors use. The same system is used for all
be aware of the importance of identifying
patients, whether stable or unstable.
and correcting the underlying abnormality
formulate daily management plans for
patients on critical care units.
Immediate management
ABCDE

INTRODUCTION Full patient assessment

Chart review
Surgical patients requiring critical care fall into History and systematic examination
two broad groups. Available results

First, there are those who are acutely unwell,

having been newly admitted or having suffered Decide and plan
an acute deterioration on the ward. These patients
require simultaneous resuscitation, diagnosis and
then definitive treatment. Stable patient Unstable/unsure

Second, there are those already on the ward or Daily Diagnosis required
within HDU who require re-evaluation and management plan Specific investigations
formulation of a management plan on at least
a twice-daily basis. Here, the aim is to ensure
that the patient is progressing, i.e. getting better. Definitive care
It is better to prevent morbidity by detecting Medical
Surgical
problems as early as possible; failure to progress Radiological
is an important sign that an incipient problem

Figure 2.1 The CCrISP system of assessment.

12
 CHAPTER 2 | ASSESSMENT OF THE CRITICALLY ILL SURGICAL PATIENT
IMMEDIATE ASSESSMENT AND
TREATMENT OF THE ACUTELY ILL
PATIENT
When assessing the acutely ill patient, your goal
is to determine what is making the patient ill and,
having identified any life-threatening problem,
to treat it immediately. Life-threatening illnesses
kill in a predictable and reproducible pattern.
When viewed in isolation, a disease process that
produces an obstructed airway will kill more
quickly than one which only produces direct
lung dysfunction, that, in turn, kills more quickly
than isolated haemorrhage or cardiac dysfunction.
Many critically ill surgical patients have linked
abnormalities of more than one vital system.
Hence, it is important not to be distracted by
obvious, but minor, factors and to assess and
treat problems systematically.
IMMEDIATE MANAGEMENT
A Airway assessment and treatment
B Breathing assessment and treatment
C Circulation assessment and treatment
D Dysfunction of the CNS
E Exposure of the patient sufficient for
full assessment and treatment
This process prioritises the order in which
assessment and treatment is carried out; although
represented as a sequence, such information can
often be obtained virtually simultaneously. For
example, the patients response to the question
How are you? can be very revealing! If the
patient is able to reply in a coherent manner,
this suggests that, at least for the moment, he
or she is in control of their airway sufficiently
13
to allow an adequate intake of breath, adequate
respiratory function to produce oxygen transfer,
adequate circulatory function to perfuse the brain
and adequate CNS function to formulate a reply.
While this is encouraging, it does not release you
from the need to perform a detailed assessment
of each of the ABCDE components of the
immediate assessment.
PRACTICE POINT
Be alert to the risks of hepatitis and HIV.
Always be alert to the risks of blood-borne
diseases in almost all emergencies there is time
and facility to adopt safety measures.
A AIRWAY
Recognition that airway obstruction is present is
based on a simple Look, Listen and Feel clinical
assessment, with immediate treatment if there is
airway compromise.
LOOK for the presence of central cyanosis,
obstructed see-saw pattern of respiration or
abdominal breathing, use of accessory muscles
of respiration, tracheal tug, alteration of level
of consciousness and any obvious obstruction
by foreign body or vomitus
LISTEN for abnormal sounds such as grunting,
snoring, gurgling, hoarseness or stridor
FEEL for air flow on inspiration
and expiration
TREAT If objective signs of airway
obstruction are present, the immediate goals
are to obtain and secure the airway to provide
for adequate oxygenation and prevent hypoxic
brain damage. Administer high flow oxygen
(1215 l/min, preferably humidified, via a
reservoir bag).
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Often, only simple methods are required to
obtain an airway such as chin lift or jaw thrust
to open the airway, suction to remove secretions
and either the insertion of an oral Guedel airway
(if tolerated) or a soft nasopharyngeal airway
(if the gag reflex is present).
If such methods are unsuccessful, a definitive
airway (an endotracheal or cuffed tube secured
in the trachea) is required. Endotracheal tubes
may be passed orally or nasally but the oral route
with the larynx visualised by direct laryngoscopy
is the most usual choice. This should not be
attempted by the untrained; in almost all
circumstances, the help of an anaesthetist should
be obtained without delay if a secured tube is
required. If the patient is in extremis, this may
be accomplished without the use of drugs. If the
patient is responsive and endotracheal intubation
is indicated, you must seek help from an
anaesthetist. Always maintain oxygenation
throughout airway manoeuvres. Attempts at
intubation without first pre-oxygenating the
patient are futile and dangerous. If endotracheal
intubation is unsuccessful, a surgical airway
should be performed: cricothyroidotomy is the
technique of choice but, again, this should not
be attempted by the untrained.
Remember that patients can be maintained with
an airway, plus bag and mask ventilation as
required, while waiting for the anaesthetist
this is often a better option for the non-expert,
particularly within hospital where skilled help is
usually rapidly available.
Protect the airway
Patients who are not fully conscious may have
an airway that they cannot protect and is only
patent intermittently. These patients may tolerate
14
and benefit from airway manoeuvres while
the cause of their reduced conscious level is
addressed.
Although unusual in the non-trauma situation,
if there is a risk of co-existing pathology of the
cervical spine, all airway manoeuvres should be
performed while maintaining manual in-line
immobilisation of the cervical spine.
PRACTICE POINT
Get help from an anaesthetist early to secure
a compromised airway.
B BREATHING
Objective evidence of respiratory distress or
inadequate ventilation can also be determined
using the clinical Look, Listen and Feel
technique, followed by immediate treatment
of life-threatening conditions:
LOOK for central cyanosis, use of accessory
muscles of respiration, respiratory rate, equality
and depth of respiration, sweating, raised JVP,
patency of any chest drains and the presence
of any paradoxical abdominal movement.
Note the inspired oxygen concentration (FiO2 )
and saturation if pulse oximetry is in use but
remember that pulse oximetry does not detect
hypercarbia
LISTEN for noisy breathing, clearance of
secretions by coughing, ability of patient to
talk in complete sentences (evidence of
confusion or decreased level of consciousness
may indicate hypoxia or hypercarbia,
respectively), change in percussion note and
auscultate for abnormal breath sounds, heart
sounds and rhythm
 CHAPTER 2 | ASSESSMENT OF THE CRITICALLY ILL SURGICAL PATIENT
FEEL for equality of chest movement, position
of trachea, the presence of surgical emphysema
or crepitus, paradoxical respiration and tactile
vocal fremitus if indicated. Percuss the chest
superiorly and laterally. Abdominal distension
may limit diaphragmatic movement and should
be looked for as part of respiratory assessment
TREAT The precise resuscitative treatment will
be determined by the cause of the respiratory
embarrassment and will be discussed later in
the chapter on respiratory failure (Chapter 4).
During the immediate assessment, you should
specifically look for signs of the immediately
life-threatening conditions: tension
pneumothorax, massive haemothorax,
open pneumothorax, flail chest and cardiac
tamponade should be identified and treated
accordingly without delay. Consider also
the diagnoses of bronchial obstruction,
bronchoconstriction, pulmonary embolism,
cardiac failure (see C Circulation) and
unconsciousness (see D Dysfunction of the
nervous system). Simple manoeuvres such as
sitting the patient up can help. However, if
the patient is tiring to the point of incipient
respiratory arrest, assisting ventilation by
bag/mask is obligatory, in conjunction with
whatever airway manoeuvres have been
necessary, until help arrives.
C CIRCULATION
Hypovolaemia should always be considered to
be the primary cause of circulatory dysfunction
in the surgical patient until proven otherwise.
Haemorrhage (overt or covert) must be rapidly
excluded. Furthermore, unless there are obvious
signs of cardiogenic shock (raised JVP particularly),
you should regard any patient who is cool and
tachycardic to have hypovolaemic shock, so
15
establish and secure adequate venous access
with at least one large (16G) cannula, send
blood off for cross-matching and other routine
tests, and initiate appropriate fluid replacement.
Start with a rapid fluid challenge of 10 ml/kg
of warmed crystalloid in the normotensive patient
or 20 ml/kg if the patient is hypotensive. You
should be more tentative in patients with known
heart failure, starting with an initial bolus of 5
ml/kg, unless you suspect that their current
problem is pulmonary oedema. Closer monitoring
may be needed in these patients.
Having identified and treated airway and
breathing abnormalities that can compromise
the circulation, life-threatening circulatory
dysfunction is recognised by looking for:
reduced peripheral perfusion (pallor, coolness,
collapsed or underfilled veins remember
blood pressure is often normal in the shocked
patient)
obvious external haemorrhage from either
wounds or drains
evidence of concealed haemorrhage: (i) thoracic
or abdominal, even when an empty drain is
present; (ii) into the gut or from pelvic or
femoral fractures; or (iii) alteration of level
of consciousness secondary to cerebral under-
perfusion.
Initially, you should assess perfusion rather than
blood pressure and institute management based
on your findings as a priority. Check the blood
pressure at an early point; it can often be
preserved in a patient with significant circulatory
problems. Marked hypotension is a late sign that
needs rapid correction.
Feel for pulses, both peripheral and central,
assessing for rate, quality, regularity and equality.
Treatment and monitoring are covered in detail
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
in Chapters 7 and 8 but should be directed
towards haemorrhage control and restoration of
tissue perfusion. You must remember that no
amount of fluid replacement will be of use in the
face of on going severe haemorrhage. Immediate
surgery to control haemorrhage may be required
at this stage as the only effective form of
resuscitation. More frequently, urgent, but non-
immediate, surgery will be needed to stop lesser
degrees of continued haemorrhage.
Shocked patients fall into three categories:
the obviously exsanguinating patient who
needs immediate definitive treatment (usually
surgery) to save their life
the unstable patient who needs rapid
resuscitation and repeated re-assessment over
a short period while the cause is identified and
treated. They may appear to respond transiently
to aggressive fluid resuscitation. Urgent
definitive treatment is essential
the patient with a relatively minor problem
who responds rapidly and adequately to a
fluid challenge and who remains stable on
re-assessment.
Re-assessment (which occurs continuously in
the initial stages) simply determines whether the
patient is responding to treatment or not. Clearly,
if there is no response (or only a transient or
inadequate response), different treatment is needed
immediately. Patients requiring large and on going
volumes of infusion are not stable, even if you
can maintain reasonable vital signs.
The fluid challenge can be repeated and colloid
solutions can be used provided you are aware of
their different distribution and side effects (see
Chapter 7, Shock). Only occasionally is it necessary
16
to give uncross-matched blood as type-specific
blood is relatively safe and can be obtained within
1020 minutes. Blood is presently the best
resuscitation fluid for the bleeding patient who
has cardiovascular instability and who requires,
as a guide, more than 15002000 ml of
resuscitation fluid.
Avoid blindly continuing to transfuse the patient
who, in reality, needs surgery. Bleeding patients
who need immediate surgery are encountered on
the ward at least as frequently as in the emergency
room patients with postoperative bleeding or
recurrent bleeding from a peptic ulcer who are
pale and shocked are typical examples. As you
resuscitate these patients, you should be calling
for senior help, cross-matching 8 units of blood
and alerting theatre, the anaesthetist and the
porters. Shocked or hypotensive patients who
are not bleeding are also seen regularly again,
do not continue to blindly fill up a patient with
litres of fluid without a clear diagnosis, a clear
plan or senior review (preferably all three!).
Most surgeons have failed to respond adequately
to continuing haemorrhage at some point during
their career so re-assess and reconsider and do
not leave a patient with inadequate perfusion
without further adequate treatment.
PRACTICE POINT
Most unwell surgical patients benefit from
administration of oxygen and fluids while
further assessment is undertaken.
Re-assess as resuscitation proceeds it often
takes more than one assessment to decide on
all aspects of the problem.
 CHAPTER 2 | ASSESSMENT OF THE CRITICALLY ILL SURGICAL PATIENT
D DYSFUNCTION OF THE CVP
In the initial assessment, a rapid determination
of neurological status is performed by examining
the pupils and by using the AVPU system:
A Alert
V responds to Verbal stimulus
P responds only to Pain
U Unresponsive to any stimulus.
Remember that the surgical patient may have
alteration of conscious level due to causes other
than a primary brain injury. Hypoxia with or
without hypercarbia and cerebral underperfusion
due to shock should have already been detected.
Recent administration of sedatives, analgesics
or anaesthetic drugs may be responsible.
Hypoglycaemia is a common and sometimes
overlooked cause that you should look for and
treat. If you have thought of all these and the
patient is still not fully conscious, re-assess and
review the ABCs: you might have missed
something.
E EXPOSURE
In order to make accurate diagnoses and allow
access to the patient for therapeutic manoeuvres,
it is essential that the patient is adequately
exposed. Be aware that this allows the patient
to become cold and exposes patients to the view
of others so respect their dignity at all times.
17
END OF IMMEDIATE MANAGEMENT
By the end of the phase of immediate assessment
and management, the patient should be showing
signs of improvement and progressing out of
immediate danger. You will very likely have
called for help and the patient may have been
to theatre or moved to intensive care before this
point is reached.
By this stage, the patient should be receiving
oxygen and intravenous fluids. If not done
already, attach a pulse oximeter, check the blood
pressure and confirm that the saturation (SaO2 )
is above 94%. Arrange pressing investigations
not already requested that are targeted and
integral to the immediate assessment (perhaps
gases, chest X-ray or ECG), insert a urinary
catheter (if appropriate) and, if necessary, alert
senior colleagues (if you have not already done
so). Before you start the next phase, quickly
re-assess the ABCs.
PRACTICE POINT
If, at any time during the immediate
assessment, the patients condition deteriorates,
you must re-assess the ABCs.
Having initiated resuscitative manoeuvres, it will
often take a few minutes for their effects to be
apparent. Vital signs may not yet be normal but,
provided the patients condition is improving,
you should use the time to continue with the
next stage of assessment in order to determine the
underlying cause of deterioration. Patients differ
(as do their problems); this system is an outline,
not an immutable series of commands. However,
if the patient is not improving, then re-assess
swiftly, get help and arrange for further immediate
treatment as appropriate.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
ASSESSMENT OF THE STABLE
SURGICAL PATIENT
In many surgical patients, particularly during
ward rounds, the vital signs will be normal. Often
this can be determined simply by looking at the
patient, by asking how they are and asking the
nurse how the patient is doing. This essentially
social introduction not only establishes rapport
and relieves anxiety but also gives information
regarding the ABCs, as it does with an acutely
ill patient. However, always ask yourself whether
the ABCs are normal; if doubt exists, a detailed
immediate assessment should be performed.
Using the system in this way can avoid simple
errors, particularly when you are tired or stressed;
it will also let you get to this point in a few
seconds with stable patients.
FULL PATIENT ASSESSMENT
Now that the patient has been immediately
stabilised, as necessary, the aim is to gather
information from a variety of sources, which
will lead to a diagnosis of current or potential
problems and, hence, to a plan of action. Your
immediate management manoeuvres are not
an end in themselves they simply buy time
to solve the underlying problems. The full
assessment incorporates a review of the charts
and available results plus a full history and
examination.
CHART REVIEWS
Inspection of the observation and fluid charts,
preferably at the end of the bed, together with
discussion with nursing and other junior medical
staff, may bring to light any recent or outstanding
18
problems. It also allows a more focused clinical
assessment to be carried out. Charts, particularly
those in HDU or ICU, may appear to carry an
overwhelming amount of data but this too can
be handled by breaking the chart into sections
and systematically noting both absolute values
and trends (Table 2.1).
It is not possible to give a comprehensive account
of management for every potential scenario but
you should consider both general and specific
aspects of care. For example, general care includes
cardiorespiratory function and fluid balance;
alternatively, following liver surgery, one might
look specifically for production or drainage of
bile, liver function tests, albumin, glucose and
clotting factor levels.
TABLE 2.1
LOGICAL APPROACH TO HDU CHARTS
R Respiratory
Respiratory rate
Inspired oxygen concentration (FiO2 )
Oxygen saturation (SaO2 )
C Circulation
Heart rate and rhythm
Blood pressure
Urinary output
Fluid balance
Intravenous lines
Central venous pressure
Cardiac output measurements
S Surgical
Special requirements of this operation
Temperature
Drainages (nature and volume)
 CHAPTER 2 | ASSESSMENT OF THE CRITICALLY ILL SURGICAL PATIENT

Check the drug chart to see what new drugs
have been given and which of the patients usual
drugs might have been forgotten: either may be
influencing the current clinical findings.
HISTORY AND SYSTEMATIC EXAMINATION
The history of the patients present illness and
subsequent treatment is just as important in
critical illness as in the rest of clinical practice.
However, the impact of co-morbid conditions
is almost as great and these are overlooked or
underestimated at considerable peril. The patient,
the case notes, nursing and junior medical staff
are the main sources of these types of information
and the appropriate source will vary from case to
case, depending on your prior knowledge of the
patient. On occasion, family and other professional
staff can also supply useful information.
The patient is then examined fully with
particular attention being paid to vital systems,
the systems or regions involved by surgery or
underlying disease and to potential problems
already highlighted. This should follow the
standard format, beginning with the hands, and
include neck, chest, abdomen and limbs. Wounds
or stomas may also require examination. The
importance of repeated clinical examination is
often underestimated by inexperienced staff,
particularly when it comes to diagnosing
incipient problems in silent areas; for example,
early signs of atelectasis are much more likely
to be detected clinically than radiologically.
Equally, we all fail to pick up on subtle signs.
Repeated examination, perhaps after 15 minutes,
helps to prevent this (Case Scenario 2.1).

CASE SCENARIO 2.1

You are on the orthopaedic ward at 3 a.m. with a trauma case when you are asked to see a 48-
year-old male patient who is tachycardic (HR 110), 12 h after a spinal cord decompression. The
main ward lights are not on, the patient is distressed and in pain and the foundation year doctor
has just started a 500ml bolus fluid challenge and prescribed more analgesia. Blood pressure is
105/75. You think the patient is a little cool peripherally but are not unduly concerned. You have
a cup of coffee and then review the patient again. You realise that, despite 500 ml of saline, his
perfusion is worse, he is oliguric and has a distended abdomen. It is now clear to you that the
patient may well have continuing surgical bleeding and that more intensive resuscitation and
consideration of urgent re-operation is required.

LEARNING POINT
Re-assessment after a short period of time or following a simple intervention often helps
clarify the diagnosis.

19
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
REVIEW OF AVAILABLE RESULTS
Available investigation results should now be
reviewed (Table 2.2). With emergencies, a great
deal of useful data may be available from
previous routine blood results microbiology
samples or recent imaging requests, so do not
overlook this source of information. On routine
ward rounds it can be better to wait at the end
of the bed for missing results than to resolve to
see them later experience suggests that these
tasks slip the memory in the busy routine. Work
out a schedule with your junior colleagues that
maximises the availability of recent results for
your main business ward rounds, including an
up-to-date file of all patients on your ward.
TABLE 2.2
REVIEW AVAILABLE RESULTS
Biochemistry profile
ABGs
Glucose level
Haematology
Blood count
Clotting
Cross-matched blood available
Microbiology
Radiology
Review reports or examine films
ECG
Return to charts and review any
necessary points
20
DECIDE AND PLAN
STABLE OR UNSTABLE?
Once you have assessed the patient and the
available information, you need to make a
decision is the patient stable or unstable?
Patients about whom you are unsure should
be managed as if unstable. Also, you should
be very cautious about assigning patients who
have been unstable, but who have just responded
to treatment, to the stable group too quickly.
Clearly, there are degrees of instability but
training yourself to make this simple decision
is important as it will focus your mind on to
one of two very different subsequent approaches.
STABLE PATIENTS DAILY PLAN
Stable patients have normal signs and are
progressing as expected. This will apply to
most patients seen on the daily ward round and,
consequently, they will not need the aggressive
immediate management for unstable patients.
It is your duty to formulate a management plan.
On the ward this will be daily (Table 2.3);
however, in HDU, 12-hourly or more frequent
assessment and planning will be needed.
Ensure that necessary therapeutic drugs, including
analgesia, are prescribed. Modify these as the
patient recovers. Check that appropriate prophylaxis,
particularly against venous thrombo-embolism,
is prescribed. Verify that routine medications are
being given (if necessary by an alternative route)
and consider what implications the co-morbid
condition or its treatment might have for present
management or prognosis.
Remember also to speak to the patient, to encourage
and reassure them. Sum up your plan with clear
instructions for your nursing colleagues and junior
staff and make or supervise an entry in the notes.
 CHAPTER 2 | ASSESSMENT OF THE CRITICALLY ILL SURGICAL PATIENT

does it need to be continued simultaneously

PRACTICE POINT with proposed investigations (usually the case)?
Plan and sum up, communicate and document. how will you achieve that?
begin any treatment or support that is
obviously necessary at once
does the patient need a higher level of care?
TABLE 2.3

DAILY PLAN SPECIFIC TARGETED INVESTIGATIONS

Investigations These are carried out as necessary to find out
Blood tests and X-rays, specialist opinions why the patient is unstable and to let you or
Removal of drains/tubes others do something about it subsequently.
These range from the simple to the very complex.
Oral intake
Usually, simple blood tests will have already
Fluid balance and prescription been sent off during the immediate management
Nutrition phase but now is the time to check. Likewise,
Requirement chest radiographs, ECGs and various cultures may
Route have already been done or may be needed now.
Is it being given? The safest way to accomplish more complex and
Physiotherapy specific investigations will differ between patients
Chest and mobility depending on the test required, the degree of
Drugs and analgesia urgency and how sick the patient is. Remember
Therapeutic (e.g. antibiotics, analgesia) the radiology department is an unsafe place for
Preventative (e.g. subcutaneous heparin) sick patients unless they have adequate critical
Routine (e.g. cardiac) care support from medical and nursing staff.
The ideal test may have to be foregone in some
Move to lower level of care
circumstances or it may be better to transfer the
patient to ICU for full support before a planned
transfer to the radiology department. Specialist
UNSTABLE PATIENTS opinions (e.g. cardiology, anaesthesia, intensive
If progress is not satisfactory, further investigation care) may be required. If you reach an impasse,
or definitive treatment will be needed. If a cause either of a diagnostic or organisational nature,
is already evident from your evaluation, treatment involve your senior colleagues. If you are unsure
can be planned directly. Inform your senior and at this stage, ask for help! However, do not give
consider whether a higher level of care is needed. up on a necessary investigation or treatment just
When the patient is unstable or you are unsure: because it is difficult to arrange, an awkward
review priorities time or beyond your expertise. Unstable patients
is resuscitation required before you begin seldom improve spontaneously between 48 a.m.
investigations (often the case)? (Case Scenario 2.2).

21
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 2.2

An elderly patient with known mild heart failure underwent endoscopy and diathermy of a bleeding
duodenal ulcer at 8 p.m. He became steadily oliguric from 11 p.m. and had two cautious fluid
challenges from the junior ward doctor. You are asked to see him at 3.35 a.m. and note he is not
well perfused and mildly dyspnoeic. You give a further 350 ml saline over 45 minutes without any
change in the patients condition. You are unsure what fluids are required and feel a central line is
needed. You are aware this needs to be performed by an anaesthetist but there is only a consultant
on call after midnight. You elect to continue with maintenance fluids until the 8 a.m. ward round
so as not to bother the consultant overnight. By then, the patient is anuric and in established
renal failure.

LEARNING POINTS
Patients do not improve magically between 4 a.m. and the 8 a.m. ward round!
Unstable patients require diagnosis and definitive treatment without undue delay
Involve senior staff if you do not have the particular skills to deal with a given problem.

Be careful to maintain momentum on busy wards, If not, a change of plan is needed!

multiple small delays at each stage can add up
to a lengthy delay in treating the underlying cause,
which can result in your previous resuscitation
being in vain.
Investigations may take some time, during which
you must ask yourself repeatedly:
is the present level of physiological support
optimal?
are we reaching a diagnosis and a definite plan
of action?
are we doing so quickly enough?
When you have attended a patient, you must
record the event in the case notes (Table 2.4). This
serves several functions writing your assessment
helps clarify your thoughts, your note tells other
staff what happened and lets them gauge the
response, you can define clear criteria for further
interventions and the note can be of medicolegal
importance.

22
 CHAPTER 2 | ASSESSMENT OF THE CRITICALLY ILL SURGICAL PATIENT

DEFINITIVE TREATMENT
TABLE 2.4
The underlying aim of critical care practice is to
WRITING YOUR NOTES begin definitive treatment of continuing pathology
or complications as quickly as possible. All the
Name in capitals, date and time,
above steps simply keep the patient alive long
pager number
enough to get this far; however, unless you treat
Assessment the real problem adequately, the patient will
Brief summary of past and present events deteriorate again and may die. Once the need for
Present clinical features intervention is clear to all, the situation may be
Response to any treatment already given irretrievable so speed is of the essence throughout.
(e.g. by foundation year doctor) Treatment may be medical, surgical or radiological
Differential diagnosis or all three: co-ordination is important. When the
Actions patient is a surgical one, you will need to play
Resuscitation performed (ABC) a leading role in co-ordinating efforts. Consider
Investigations and opinions where non-operative treatment should best be
Treatment carried out, by whom and what support will be
necessary. If the patient is transferred, especially
Communications to relatives, staff,
to an area unfamiliar with surgical patients
seniors, etc.
(e.g. coronary care unit), detailed instructions will
Review need to be written in the case notes and frequent
By you review will be necessary to ensure that other
By others surgical aspects of care continue to be delivered
Parameters for change even though the staff are unfamiliar with them.

RE-ASSESSMENT
Finally, once any treatment has been instituted,
whether simple fluid therapy or a complex surgical
operation, you must re-assess the patient to
ensure that they have responded to the treatment.
The necessary time frame for doing this will
depend on the urgency of the case.
If they have not responded adequately, then you
need to look all the harder for a different cause
to treat. Re-assessment is the final step and, if
necessary, the first step in repeating the whole
process.

23
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

SUMMARY
This system will let you assess all your patients
Immediate management
in a similar way. It is the system that many
ABCDE
senior surgeons and intensivists have used
subconsciously for a long time, just in written
form. With practice, the use of a system will let Full patient assessment
you assess patients without overlooking simple Chart review
and potentially disastrous things and it will serve History and systematic examination
Available results
as a framework whereby you can apply your
theoretical knowledge to clinical problems.
using a structured system to assess critically Decide and plan
ill patients reduces serious omissions
identify those in need of immediate
life-saving resuscitation assess and treat Stable patient Unstable/unsure
them simultaneously Daily Diagnosis required
reach a diagnosis that accounts for management plan Specific investigations
clinical deterioration
formulate and institute a plan of definitive
treatment Definitive care
investigations should be selective and carried Medical
out in a safe environment Surgical
Radiological
repeated clinical assessment is the cornerstone
of good practice it identifies things missed
first time around and tells you whether the Figure 2.1 The CCrISP system of assessment.
patient is getting better
inform and involve your senior colleagues
at an early stage
consider the level of care necessary at
each stage
communicate and document at all times.

24
3
Airway and
tracheostomy
management

25
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the basic principles of airway
management
recognise the indications for tracheostomies
in critically ill patients and the indications
for their removal
understand how to deal with some common
complications of tracheostomies.
AIRWAY MANAGEMENT
The commonesty reason for admission to an
ICU is to provide airway and ventilatory care
to critically ill patients who are unable to
maintain their own airway and normal respiratory
functions. The early recognition of an airway
or ventilatory problem together with early
appropriate treatment will often prevent further
deterioration and is the basis of effective
resuscitation. Many more patients on surgical
wards exhibit signs of respiratory compromise
and their effective management is a sizeable
and important part of surgical critical care.
As outlined in Chapter 2, you should look
specifically for an airway problem when assessing
every patient. Often, the patient will respond
verbally but, if not, you should suspect airway
compromise in any obtunded patient. Alteration
in the level of consciousness, for whatever reason,
will result in loss of airway control, decreased or
loss of protective gag and/or laryngeal reflexes
and increased risk of aspiration of gastric contents
into the lungs.
26
Problems with the airway are generally quite
intimidating for surgical trainees: an unconscious
patient with no airway must be resuscitated
quickly to prevent hypoxic brain damage.
Remember the ABC approach of the CCrISP
algorithm also applies in cases of apparent airway
problems. You can review how airway management
fits into this system in Chapter 2.
The patient with airway and/or breathing
difficulties may be easily recognised if they are:
dyspnoeic, tachypnoeic or apnoeic
unable to speak in complete sentences
using accessory muscles of respiration
centrally cyanosed
sweaty and tachycardic
showing a decreased level of consciousness
or becoming agitated and difficult to control.
There are two golden rules to airway management:
(i) always give oxygen in the highest concentration
possible; and (ii) use simple methods first.
TECHNIQUES OF AIRWAY CONTROL
If the patient is still breathing, use high flow
oxygen masks (e.g. Hudson mask) with a reservoir
bag (Fig. 3.1). During resuscitation, you should
not worry about the possibility of depressing
ventilation by giving high concentrations of oxygen
to a patient who normally requires a hypoxic
drive to produce adequate ventilation. Hypoxia
kills people quicker than loss of respiratory drive
and the condition is rarely seen in surgical patients.

Figure 3.1 High flow oxygen mask with reservoir bag.
Apply a pulse oximeter to allow you to assess
that oxygen administration is improving the
patients saturations. Once the patient has
stabilised, the oxygen concentration can be
decreased to maintain adequate saturations:
pulse oximetry can guide this. Remember that
pulse oximetry does not indicate hypercapnia.
ESCALATING AIRWAY SUPPORT
In increasing measure, airway support can be
achieved by: (i) chin lift/jaw thrust; (ii) suction;
(iii) oral Guedel airway or nasopharyngeal airway
if gag reflex present; (iv) laryngeal mask or
endotracheal tube; and (v) surgical airway.
Basic manoeuvres without airway adjuncts are
often sufficient to improve gas exchange through
a compromised airway. If not, an oral Guedel
airway should be inserted (Fig. 3.2). This is sized
from the angle of the mandible to the mouth, and
inserted upside down and rotated as it is inserted.
27
CHAPTER 3 | AIRWAY AND TRACHEOSTOMY MANAGEMENT
Have suction on hand at all times. A nasopharyngeal
airway may be inserted if the patient has a gag
reflex.
In situations of airway compromise, call for
help early. In particular, seek anaesthetic/critical
care help at any point if you are unable to
cope or think you may reach the limits of your
competency. Patients who are semiconscious
and unable to tolerate an oral airway will not
tolerate endotracheal intubation or laryngeal
mask insertion without additional sedation and
so you must seek additional help to secure the
airway. If the patient is apnoeic or has very
shallow respiration then ventilation using a
bag/valve /mask system is required (Fig. 3.3).
This can usually maintain the patient until an
anaesthetist arrives. With appropriate training,
attempting to insert a laryngeal mask airway
can often be simpler, quicker and easier than
attempting intubation. If you do decide to attempt
intubation, you should keep in mind the risk of
regurgitation and aspiration of stomach contents
and apply cricoid pressure prior to laryngoscopy.
Neither technique should be attempted by the
inexperienced trainee help must be sought!
If you try to intubate the patient and fail, or if
you are unable to ventilate the patient manually
or with a laryngeal mask airway, then you are
committed to performing a surgical airway by
either needle or surgical cricothyroidotomy in
order to ensure life-saving oxygenation and
ventilation. The techniques of airway management
are covered in the Advanced Trauma Life Support
(ATLS) course and will not be covered in further
detail in the CCrISP course.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Figure 3.2 Geudel airway.
Figure 3.3 Bag/valve/mask system.
28
TRACHEOSTOMY
Tracheostomy is commonly performed in
patients in the ICU, mostly using variations of
the Seldinger guidewire technique as a planned
bedside procedure. There is currently no evidence
that one technique is superior to the other, and
often the chosen technique will depend as much
on local practice as patient factors. Indications
for tracheostomy are listed in Table 3.1.
TABLE 3.1
INDICATIONS FOR TRACHEOSTOMY
IN CRITICALLY ILL PATIENTS
Weaning from mechanical ventilation
Bronchial toilet (excessive secretions,
poor cough)
Protect the airway (e.g. following CVA)
Maintain the airway (e.g. upper airway
obstruction)
Tracheostomies are increasingly being performed
early in a patients stay on the ICU and, in some
hospitals, patients with tracheostomies are being
managed on non-ENT wards. It is, therefore,
important for surgeons to be aware of, prevent and
deal with the common complications of tracheostomy.
TYPES OF TRACHEOSTOMY
Tracheostomy tubes can vary depending on the
needs of the patient and the problems the
tracheostomy is intended to overcome. They are
constructed from either a form of plastic or metal.
Documentation of the type of tube and size should
be in the patients notes and this should always
be checked where possible. Other features of
tracheostomy tubes are listed in Table 3.2 and
illustrated in Fig. 3.4.
 CHAPTER 3 | AIRWAY AND TRACHEOSTOMY MANAGEMENT

TABLE 3.2

FEATURES OF TRACHEOSTOMY TUBES

Tracheostomy feature Further information

Cuffed versus uncuffed Cuffed tubes are required for mechanical

Single lumen versus inner cannula
Fixed versus adjustable flange
Fenestrated versus non-fenestrated
ventilatory support but do not allow speech
Inner cannula can be removed for cleaning
without loss of the tracheostomy as the
outer tube remains in place. Safer long term
Adjustable flange tubes can be used to
overcome short-term anatomical problems
such as swollen neck but are not suitable
for longer term use
Fenestrations allow patients to talk with
a tracheostomy tube in situ. Not used in
ventilated patients

Information on tube size should be located on

the flange; unfortunately, there is no uniformity
of tracheostomy tube size with regard to length
and dimensions so this needs to be checked for
each type of tube. As a general rule, most adult
females can accommodate a tube with an outer
diameter of 10 mm, while for most men a tube
with an outer diameter of 11 mm is suitable.
Selecting appropriate tube size is important to
maximise the internal tube dimensions and reduce
the work of breathing through the tube. However,
an over-sized tube can cause pressure necrosis
and damage the tracheal mucosa. A tracheostomy
tube that is too small will need over-inflation of
the cuff to prevent accidental displacement.

Figure 3.4 Selection of tracheostomy tubes.

29
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
WARD MANAGEMENT OF
PATIENTS WITH A TRACHEOSTOMY
Management of tracheostomies on the ward is
usually straightforward, provided simple principles
are followed:
humidification and regular suction are
essential: it is often lack of basic toileting of
the airway that leads to tracheostomy blockage
apply the CCrISP algorithm when asked to
deal with a tracheostomy problem or review
the continuing need for one
determine when the procedure was performed
and what type of tracheostomy the patient
received. Tubes should not be changed within
3 days of a surgical procedure, and ideally not
within 7-10 days of a percutaneous procedure,
to ensure that the track has formed properly
on the wards, single lumen tubes are generally
unfavourable due to the risk of blockage.
These should be replaced with a tracheostomy
with a removable inner tube to facilitate
cleaning as soon as it is safe to do so.
PRACTICE POINT
Tracheostomy tubes should only be changed
by staff who have the necessary competencies.
If you have not had relevant training you will
not have competency in this area and should
not plan to undertake the procedure
unsupervised.
30
COMPLICATIONS OF TRACHEOSTOMY
The commonest major complications are blockage,
displacement and haemorrhage.
Blockage or displacement
A blocked or displaced tracheostomy tube
generally presents with respiratory compromise.
Always use the CCrISP algorithm: remember
there may be other cardiorespiratory reasons
for breathing difficulties, which may be missed
without a systematic approach. A partially
displaced tracheostomy tube is just as dangerous
as a blocked or completely removed tube. The
key factor to determine is if the airway is patent.
If the tube is displaced, the patient may be breathing
through their nose or mouth. It will usually be
safer to remove a partly dislodged tube. The
patient can be given oxygen via facemask and
monitored in the short term with pulse oximetry.
If there are problems once the tracheostomy has
been removed, you should not try to replace it.
Maintain the airway by other methods until
experienced help arrives.
If you bag/mask ventilate a patient after removal
of the tracheostomy tube, air will escape from the
stoma and you will need an assistant to occlude
the stoma by hand and an occlusive dressing to
reduce the leak.
If the tube is partially blocked, the patient may
still be able to breathe through it with difficulty:
encourage the patient to cough as this may
dislodge any blockage
pass a suction catheter down the tube
oxygen should be given via the tracheostomy
and also via a facemask
if the tube has an inner cannula, this should
be removed and changed

if the tube has a single lumen tube and a
suction catheter can be passed, it must be
partially patent: the patient can be monitored
and given oxygen until the arrival of
expert help
if the patient cannot breathe spontaneously
via the stoma, establish an airway by other
means. Call for help at this point if you have
not already done so!
Haemorrhage
Tracheostomy site bleeding on the ward may
occur because of erosion of blood vessels in
and around the stoma site. Bleeding may settle
with conservative management. However, if it
results from erosion of a major artery in the root
of the neck, the bleeding will be massive and is
a life-threatening emergency. This should be
managed as follows:
try not to panic, call for help (anaesthetic and
surgical) and adopt the CCrISP algorithm
reassure the patient
inspect the stoma site for any obvious bleeding
point and apply manual pressure
if still bleeding, infiltrate any obvious bleeding
point with dilute adrenaline (1:80,000 to
1:200,000)
if no obvious bleeding point, infiltrate the
stoma margins generally
check full blood count and a coagulation
screen. Correct any abnormalities and ensure
blood for transfusion is available
bleeding may be temporarily stemmed by
applying pressure to the root of the neck in
the sternal notch or by inflating the cuff
slowly, taking care not to burst it. Depending
on the type and size of the tube, this may
need a volume of 1035 ml
31
CHAPTER 3 | AIRWAY AND TRACHEOSTOMY MANAGEMENT
call for senior surgical help if you have not
already done so as the patient needs surgical
exploration, preferably by an ENT or
maxillofacial surgeon.
TRACHEOSTOMY TUBE REMOVAL
Reviewing the continuing need for a tracheostomy
should be part of the daily patient plan. It is
important to remove a tracheostomy as soon as
it is no longer required and the initial indication
for its presence has passed. If the patient can
cough, expectorate, phonate and protect the
airway with the cuff deflated, and is maintaining
good oxygen saturations on minimal oxygen
concentrations, the prospects for decannulation
are good. The best time for decannulation is
usually in the morning as the patient has rested
overnight and their condition can be observed
during the remainder of the day. Some hospitals
are able to provide assessments from speech and
language therapy as to swallowing and laryngeal
competence but this is not universal. The use of
specialised tracheostomy tubes requires input
from your ENT or ICU colleagues.
If you do not know how to replace/change a
tube, always ask for help before you start.
Depending on the hospital, this may be obtained
from a critical care out-reach team, anaesthesia,
physiotherapy or other staff.
As a general rule, the following steps are necessary:
ensure that the appropriate equipment is
available (Table 3.3)
monitor the patient with pulse oximetry as
a minimum. Be aware that suctioning can cause
bradycardia
ensure the patient is receiving supplemental
oxygen via the tracheostomy mask
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
inform the patient about the procedure and
ensure he or she understands
position the patient so that he or she is
comfortable with the neck slightly extended
if possible
suction the tube using an endobronchial
suction catheter
deflate cuff after ensuring patients pharynx
is empty with oral suctioning
remove the tube
after decannulation, dress and occlude
the stoma with sterile gauze covered with
an occlusive tape dressing
give the patient supplemental oxygen via
a facemask or nasal cannulae
observe the patient for signs of respiratory
distress.
TABLE 3.3
EQUIPMENT FOR REMOVAL OF
A TRACHEOSTOMY TUBE
Operational suction unit with suction
tubing attached and Yankaeur sucker
Endobronchial suction catheters
Gloves, aprons and eye protection
Spare tracheostomy tubes of the same
type as inserted: one the same size and
one a size smaller
Tracheal dilator forceps
Self-inflating reservoir bag and tubing
Catheter mount
Tracheostomy tube holder and dressing
10 ml syringe (if tube cuffed)
Resuscitation equipment
32
Risks of tracheostomy removal include airway
obstruction, aspiration, ventilatory failure, sputum
retention and difficulty with oral re-intubation
if required.
SUMMARY
there are two golden rules to airway
management in surgical patients always give
oxygen in the highest concentration possible
and use simple methods for airway control first
seek anaesthetic/critical care help at any point
if you are unable to cope or think you may
reach the limits of your competency
common complications of tracheostomy in
ward patients are accidental displacement,
blockage and haemorrhage
surgeons need to be aware of and be able to
deal with these complications and how to avoid
them by appropriate ward-based management.
Be aware of when and who to call for
additional expert help.
FURTHER READING
Standards for the care of adult patients with a
temporary tracheostomy. Intensive Care Society,
July 2008. Available at <http://www.ics.ac.uk>.
Advanced Trauma Life Support for Doctors.
ATLS Student Course Manual. 8th edn. Chicago,
IL: American College of Surgeons; 2008.
4
Respiratory
compromise in
the surgical patient

33
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the importance of respiratory
failure and its prevention
recognise the patient with respiratory failure
and the need for support
provide a management approach to
respiratory failure
be familiar with common methods of
respiratory support
understand the basic concepts of mechanical
ventilation.
INTRODUCTION
Respiratory failure is an acute or chronic failure
of oxygenation, manifesting as a PaO2 of less than
8 kPa, due to inadequate pulmonary gas exchange.
A PaO2 of 8 kPa is the point on the oxygen
dissociation curve when rapid desaturation occurs
if there is any further fall in PaO2 (Fig. 4.1).
Respiratory failure represents the commonest
cause of a decreased level of consciousness in
general surgical patients and is classified
depending on the CO2 level:
Type I failure failed oxygen uptake leads
to hypoxia (PaO2 of less than 8 kPa: normal
range, 10.613.3 kPa) but normal or reduced
PaCO2 (normal range, 4.76.0 kPa)
Type II failure failed oxygen uptake and
carbon dioxide removal leads to hypoxia and
hypercarbia (PaCO2 of greater than 6.7 kPa).
34
There are a number of common causes of
respiratory failure in the surgical patient, which
can be classified into three broad groups:
Acute fall in functional residual capacity
without pulmonary vascular dysfunction
includes central or myoneural disorders,
failure of chest mechanics after trauma or
other processes that render the lungs stiff and
non-compliant. Acute postoperative atelectasis,
sputum retention, pneumonia or depression
of respiration by analgesic, sedative or
neuromuscular blocking drugs fall into this
category. Frailty and malnutrition contribute
Acute fall in FRC with pulmonary vascular
dysfunction includes left ventricular failure,
fluid overload, pulmonary hypertension,
pulmonary embolism, neurogenic pulmonary
oedema or ARDS
Airflow obstruction including increased lung
volume states such as chronic obstructive
pulmonary disease, asthma or other airflow
obstruction.
Factors that increase the risk of respiratory
problems include:
history of pre-existing respiratory disease,
such as asthma, COPD and obstructive
sleep apnoea
smoking
thoracic surgery
upper abdominal surgery
obesity
elderly.
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT

Aim to oxygenate the patient using high

100 flow oxygen masks of suitable oxygen delivery
90 percentages if the patient is still breathing.
80 Remember, during resuscitation, you should
70 not worry about the possibility of depressing
60
ventilation by giving high concentrations of
SaO2 (%)

oxygen to a patient with chronic pulmonary

50
disease who normally requires a hypoxic drive
40
to produce adequate ventilation having become
30
habituated to a high level of arterial carbon
20 dioxide. If the patient needs oxygen that badly
10 you should give it!
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13 Apply a pulse oximeter. Once the patient has
PaO2 (kPa) stabilised, the rule is to give the minimum
added oxygen to achieve the best oxygenation.
Figure 4.1 The oxygen haemoglobin dissociation curve. Below a
PaO2 of 8 kPa the slope drops away steeply. Keep the saturation
> 94% to ensure the PaO2 is above 8 kPa!
PULSE OXIMETRY
Pulse oximetry has become a central tool in
IMMEDIATE ASSESSMENT the monitoring of critically ill surgical patients.
AND MANAGEMENT It represents a continuous method of monitoring
Although the precise definition of respiratory oxygen saturations, not absolute oxygen levels
failure is based on ABG criteria, the initial or ventilation.
assessment and management approach should Understanding the mechanism will make you
follow the systematic approach of the CCrISP aware of the limitations. Pulse oximetry works
algorithm. by combining two principles based on light
Remember the ABCs. An unconscious patient with transmission and reception through the tissue.
no airway must be resuscitated quickly to prevent First, the probe detects pulsatile flow
hypoxic brain damage. Review airway management plethysmographically. Second, it differentiates
in Chapters 2 and 3. between oxygenated and reduced haemoglobin
Patients with respiratory failure may be easily by their differing light absorption. Signal
recognised if they are: processing produces a display of heart rate
dypnoeic, tachypnoeic or apnoeic and arterial oxygen saturation (SaO2 ).
unable to speak in complete sentences Remember that the saturation does not equate
using accessory muscles of respiration to the partial pressure (which is responsible for
centrally cyanosed gas exchange) the oxygen dissociation curve
sweating and tachycardic, and/or in Fig. 4.1 links these parameters. Note that
showing a decreased level of consciousness. SaO2 of 94% often equates with a PaO2 of

35
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
approximately 8 kPa so it is advisable to aim to
keep the SaO2 above 94% and to set the alarms
accordingly. There is a delay of around 20 seconds
between actual and displayed values.
The pulse oximeter does not detect hypercarbia
or acidosis these require blood gas analysis.
The pulse oximeter is fooled by carboxyhaemoglobin
into giving an erroneously high reading. Other
factors that impede accurate pulse oximetry
include:
movement: shivering, rigors, tremor, agitation
peripheral vasoconstriction shock, hypothermia
dirty skin/pigmentation including jaundice/
nail varnish
cardiac arrhythmias
profound anaemia
diathermy
bright lights
when the SaO2 is lower than 70%.
FULL PATIENT ASSESSMENT
CHART REVIEW
Chart examination may reveal changes in
respiratory rate, temperature, pulse rate, blood
pressure, change in colour or amount of sputum
produced, change in level of consciousness or
a fall in oxygen saturation or deterioration in
ABG if previously recorded. Fluid balance
charts should be examined for signs of fluid
overload. A deteriorating trend in any of these
physiological variables is an essential diagnostic
tool and accurate charting cannot be over
emphasised.
HISTORY AND SYSTEMATIC EXAMINATION
You should rapidly review the patients history
in an effort to determine the likely source of
36
respiratory difficulty. The patient may be a known
asthmatic, chronic bronchitic or may recently
have received a large dose of opiates. If this
information is obtainable from the nurses, you
can be simultaneously examining the patient.
The examination should initially be clinical,
based on simple Look, Listen and Feel techniques
described in the assessment chapter and aimed at
detecting the physiological changes of developing
respiratory failure.
AVAILABLE RESULTS
Full blood count: correction of anaemia will help
to improve oxygen delivery to the tissues if the
haemoglobin is less than 10 g/dl. Over-transfusion,
conversely, brings the risk of fluid overload and
increased blood viscosity. An elevated white cell
count may indicate concurrent infection that may
be pneumonic in origin.
The urea and electrolytes may give some
indication of fluid and renal status.
ABG sampling is the single most useful blood
test in relation to respiratory failure. You should
be familiar with the practical skill of sampling
and the interpretation of these results. The
interpretation of ABGs is outlined in Chapter 5.
Remember to treat the patient as a whole and
not to act only on the blood gases in isolation
from the clinical findings.
The ECG will provide information regarding
the presence or absence of myocardial ischaemia,
rhythm and rate, abnormalities of which may
be responsible for the onset or worsening of
respiratory failure. Cardiac and respiratory
physiological variables are inseparable when it
comes to assessment and treatment of respiratory
failure, and further investigations of cardiac
function such as echocardiography or cardiac
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT
output or index estimations may be appropriate
at a higher level of care.
The plain chest X-ray remains a valuable diagnostic
tool but transfer of the unstable patient to the
radiology department is dangerous and should not
delay treatment. Radiographic changes often lag
behind the clinical changes and it is important to
treat the patient, not the X-ray. Interpretation of
chest X-rays must follow a systematic approach
as described in Table 4.1.
Pre-operative lung function tests (peak expiratory
flow rate, vital capacity and FEV1 ) are useful in
predicting the patient at risk although a patients
ability to climb a flight of stairs in one go or to
conduct everyday tasks also provides valuable
information.
Infection is the most common cause of respiratory
failure and samples of sputum and blood for
culture should be obtained preferably before
commencing antibiotic therapy. If the patient
is already on antibiotics, these should be taken
before the next dose when antibiotic blood levels
are at their lowest. In the intubated patient, sputum
samples can be taken by BAL. These give better
results since they are uncontaminated by upper
airway flora.
STABLE PATIENT
DAILY MANAGEMENT PLAN
Frequent assessment of all surgical patients,
but especially those at high risk, is important.
Routinely assess respiratory rate, SaO2 along with
oxygen requirements, cyanosis, ability to cough
and deep breathe, looking for signs of respiratory
distress, sweatiness and tachycardia and formal
examination of the chest. If there any concerns,
consider the investigations outlined above.
37
Prescribe humidified oxygen therapy by
mask at an appropriate concentration. Monitor
clinical signs (especially respiratory rate), oxygen
saturation and ABGs. For patients with lower
oxygen requirements, nasal cannulae may be
used, but remember that oxygen should be
administered to patients to keep their SaO2
above 94%. Communicate with nursing staff
and ensure that they are aware of the increased
frequency of desired observations to be made.
Physiotherapy review should be sought for all
patients at risk of, or developing, respiratory
problems. Important aspects to be considered
are patient positioning, mobilisation, exercises to
encourage deep breathing, suction of respiratory
secretions using nasopharyngeal airways,
techniques such as percussion and use of devices
such as incentive spirometry.
Ensure patients are on any routine prescriptions
they have for respiratory disease such as inhalers
and nebulisers. Consider use of nebulised saline
to loosen secretions. If a patient develops wheeze
(which can occur in the absence of previous
respiratory disease), prescribe nebulised salbutamol
and ipratropium. Increasingly, patients are using
home NIV or CPAP. Ensure that any patient
who uses these devices brings them into hospital
with them and that staff who will be looking
after them are familiar with their use. Adequate
analgesia is important to enable patients to
cough and deep breathe. Conversely, over-use
of opiates leads to narcotisation, and airway and
respiratory compromise.
Set parameters beyond which staff must call for
further medical opinion. Commence hourly urine
output monitoring if the patient is catheterised
and enforce meticulous fluid balance and
microbiological surveillance (sputum and blood
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

cultures). Monitor respiratory rate, SaO2 , FiO2 , BP, hourly. Increasingly, MEWS charts are being used.
heart rate, temperature and AVPU score. For most Abnormalities in observations should be reported
surgical patients, 4-hourly observations are to critical care out-reach teams, who will help
appropriate but, if you are concerned, increase to with liaising with critical care and offer advice.

CASE SCENARIO 4.1

A 45-year-old man had a laparoscopic gastric bypass 2 days ago. His BMI is 45 kg/m2, and he
has a history of obstructive sleep apnoea but has refused home CPAP because of poor tolerance.
He has a history of chronic pain problems and normally takes regular paracetamol and oramorph
PRN. You are called to see him because his saturations are 90% and he is complaining of pain.
He is maintaining an airway and immediate assessment reveals a temperature of 37.3C, respiratory
rate of 24 and SaO2 of 90% on room air. He has not been out of bed since the operation as there
is no suitable chair. He also has NIDDM and hypertension. He is cyanosed but well perfused. You
review him in detail and find that he has not been receiving his normal analgesia, no oxygen
therapy had been given for 6 h and that he had not seen the physiotherapist today. He has poor
air entry bilaterally, particularly at the right base. Blood gases now show a mild respiratory acidosis
and a PaCO2 just above the upper limit of normal. You prescribe humidified oxygen to maintain
his saturation above 95% and start regular nebulised salbutamol as he uses salbutamol as necessary
at home. A CXR is requested, which reveals atelectasis at both bases (Fig. 4.2). You arrange for
immediate review by the on-call physiotherapist and by the pain team. The physiotherapist obtains
a sputum sample for culture but, as this looks clear and as he has a normal white cell count,
you elect not to start antibiotics at present. You review him 1 h later, confirm that his improved
analgesia has allowed him to increase his air entry and clearance of secretions and thereby,
oxygenation. The blood gases have improved. You discuss the case with the nurse and agree the
necessary frequency of observations and parameters of saturation, respiratory rate and pain score
that would necessitate further urgent medical review. You plan to review in any event at 8 a.m.
to discuss with (and feed back to!) the patients own team.

LEARNING POINTS
predict the patients at risk and establish the correct level of care from the outset
regular nursing observations and medical review once daily is not enough in some cases
use preventative techniques including chest physiotherapy, nebulised saline, monitored
humidified oxygen, adequate analgesia and sputum culture liberally.

38
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT

Figure 4.2 CXR confirmed to be a recent film of the patient in Case Scenario 4.1. There is basal shadowing
suggestive of marked atelectasis and no other obvious pathology.

PRACTICE POINT PREVENTING RESPIRATORY

The frequency with which early chest problems DETERIORATION FOLLOWING SURGERY
are encountered cannot be overemphasised, identify those at risk
nor can the importance of examining the chest examine and assess
routinely and adopting simple preventive chest physiotherapy
measures liberally. nebulised saline
humidified oxygen titrated dose
adequate analgesia
sputum culture
re-assess regularly.

39
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

PRACTICAL SKILL:
INTERPRETING CHEST RADIOGRAPHS

OBJECTIVES
learn a system for examining chest
radiographs in the critically ill
be aware of the complementary information
provided by clinical and radiographic
A A
examination.

Figure 4.3a Chest x-ray showing the line method of assessment.

The CXR is one of the most frequently ordered
investigations in the management of the critically Trachea
ill. In many cases, abnormal signs will be picked Superior vena cava
up earlier on clinical examination as radiographic
appearances tend to lag behind the clinical Aortic arch

findings. The CXR offers valuable confirmatory Left hilium

Right hilium Pulmonary artery
and complementary diagnostic evidence (or and right
main bronchus
branches fan out
reassurance). The aim here is not to list exhaustively Right atrium
Left atrium

the clinical scenarios and diagnoses where it may Lung peripheries

be of help, but rather to teach a system of reading

Cardo-phrenic Left ventricle
a CXR. angle

Use a routine when looking at chest X-rays:
you may miss other pathology if you do not.
The most useful chest view for assessing the heart
is a straight, erect PA, taken at full inspiration.
This type of radiograph is more likely to give a
true indication of heart size than the portable AP
film which may suggest cardiomegaly. Be aware
of which type you are looking at and remember
to check name, date and time. Compare with
previous films.
Your routine should be:
note overall shape of the chest and obvious
abnormalities
use a system to assess the CXR fully.
One system is the line method (Fig. 4.3a).
Costophrenic angle
Figure 4.3b Diagrammatic representation of a CXR.
Draw a line across the lower part of the CXR to
include the costophrenic angle as shown (AA).
The line passes through the structures to be
examined in order:
soft tissues: look for air (surgical emphysema),
foreign bodies or disruption of contours
bony structures: use the Collegiate mnemonic
RCSS comprising ribs, clavicles, scapulae,
sternum
lung markings: do they extend to the chest
wall? Is there pneumothorax or haemothorax?
Trace around the edge of the pleural cavity to

40
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT
avoid missing a small pneumothorax. Is the
volume of parenchyma increased (COAD, lots
of ribs visible) or reduced (poor respiratory
effort, abdominal distension)
examine the lung fields for opacities
double check the costophrenic angles for fluid
(erect film?)
is there air beneath the diaphragm (erect film?)
or any obvious intra-abdominal abnormality to
investigate specifically, such as distended bowel
note tracheal position and heart size. Trace
round the mediastinum and check the location
of any tubes or lines. The width of the
mediastinum should be noted but may be
unreliable. Combined with a history suggestive
of aortic aneurysm, dissection or trauma, a
second opinion should be sought immediately.
AIR BRONCHOGRAM
A bronchus is not normally visible if surrounded
by aerated lung since both are equally radio-opaque.
Anything that causes the normal lung tissue to
lose its aerated property will produce a difference
in opacity and the bronchus, provided it still
contains air, will be visible. Thus, the presence
of an air bronchogram suggests oedema, infection
or other infiltrates in the surrounding lung tissue.
KERLEY B LINES
These are horizontal lines that meet the pleural
surface at right angles. They tend to be about 12
cm long and 12 mm thick. They are caused by
increased fluid or tissue within the intralobular
septa.
BRONCHITIS AND EMPHYSEMA
Bronchitis and emphysema can be present with
little or no CXR abnormalities. What may be present
is increased lucency of the lung and regional or
41
general loss of vascularity in the peripheral lung
fields. The lung fields are increased in size.
PLEURAL EFFUSION
A small effusion may only produce a blunting
of the costophrenic angle. A large effusion will
produce evidence of lung compression, usually
respiratory problems, and the mediastinum may
be displaced to the opposite side and the
diaphragm flattened on that side. It is important
to be aware that, with an X-ray taken with the
patient supine, an effusion may show only as
a faint diffuse opacity spread over the lung field.
This is because the fluid is spread thinly over
a wide area. Repeat the X-ray with the patient
having been sat up for 15 minutes or obtain an
ultrasound scan. An effusion due to a cardiac
disorder tends to be bilateral.
CONSOLIDATION
Consolidation will not produce a mediastinal
shift unless there is significant collapse when the
mediastinum will be drawn over to the side of
the lesion.
PERICARDIAL EFFUSION
There are many reasons for an enlarged cardiac
silhouette, which can be apparent or pathological.
The most common pathological reasons include
ventricular hypertrophy, pericardial effusion and
ventricular aneurysm. An effusion may produce
an outline that is globular in appearance but
hypertrophy of the left ventricle can do the same.
Left atrial enlargement can produce a straightening
of the left cardiac border. A significant pericardial
effusion is likely to produce evidence of tamponade
with poor cardiac function and raised central
venous pressure. If in doubt, ultrasound will
confirm the diagnosis.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Cardiac failure may give rise to a variety of signs
including upper lobe blood diversion, cardiomegaly,
pleural effusions, Kerley B lines and parenchymal
shadowing (diffuse or hilar bats-wing).
MANAGEMENT OF RESPIRATORY
FAILURE AND COMPROMISE
The treatment plan for managing respiratory
failure follows a step-wise increase/decrease in
support depending on its severity (Fig. 4.4).
Adjunctive
therapies
PEEP and
recruitment
Intubation
and ventilation
NIV
Mask/tracheal
CPAP
Mask oxygen
therapy
Increasing severity of respiratory failure
Figure 4.4 Treatment plan for managing respiratory failure.
During initiation of treatment, you start at the
left of the scale and progress to the right as
determined by your assessment of the patients
response.
Only conventional mask oxygen therapy is possible
on the majority of surgical wards. Fixed delivery
oxygen masks are available up to an inspired
oxygen concentration of 60%, an FiO2 of 0.6.
All oxygen delivery systems should be humidified.
Otherwise the dry, cold gas, may contribute
towards thickening of the patients secretions and
promote sputum retention. Nebulised 0.9% saline
(with bronchodilators if indicated) and regular
42
treatment from a respiratory physiotherapist may
prevent worsening of incipient respiratory failure
if they are used early.
The response of the patient is assessed according
to the improvement of clinical status, oxygen
saturation and ABG analyses. If the patients
condition does not improve with increased
inspired oxygen concentration up to 60%, then
you have a very unstable patient and further
diagnosis and definitive treatment are required.
This will involve expert help and the safe transfer
of the patient to a higher level of care.
Even if the patient responds to supplemental
oxygen therapy and the ABGs improve, you
must remember that oxygen is only one aspect
of treatment you must treat the underlying
cause of the respiratory failure.
TREAT THE CAUSE OF RESPIRATORY FAILURE
Supportive and definitive treatments are needed.
Use appropriate antibiotics, physiotherapy,
diuretics, bronchodilators and cardiac or other
drugs as necessary. Basal signs may indicate
continuing abdominal pathology (e.g. subphrenic
abscess). Systemic factors influence respiratory
function (e.g. mobility, nutrition) it is important
to treat these too.
Review the patients requirement for and response
to analgesia; either too little or too much can be
a factor in preventing adequate clearance of
secretions by inhibiting coughing and by limiting
the patients tolerance of physiotherapy.
Where sputum clearance is the primary problem,
a mini-tracheostomy should be considered.
Do not assume that confusion or depressed level
of consciousness are due to the effects of opiate
analgesia. Hypoxia may cause an acute confusional
state and hypercarbia may lead to obtundation.
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT

RE-ASSESS
Detect failure of improvement or deterioration: FAILURE OF MASK OXYGEN THERAPY
persisting or worsening signs and symptoms of AT HIGH FiO 2 MAY BE INDICATED BY:
respiratory failure necessitate further immediate increasing respiratory rate
management and safe transfer to a higher level increasing distress, dyspnoea, exhaustion,
of care. sweating and confusion
oxygen saturation 80% or less
DETECTING SIMPLE OXYGEN FAILURE (this may be a late sign)
It is essential to be alert to this situation as it PaO2 less than 8 kPa
is common, can be rapidly fatal and requires PaCO2 greater than 7 kPa.
a prompt change in management.

CASE SCENARIO 4.2

A 62-year-old woman with chronic bronchitis is 4 days postoperative following a right abdominal
nephrectomy. This morning she was noted to be tachypnoeic, pyrexial and with reduced air entry,
bronchial breathing and dullness to percussion at the right lung base. Her FiO2 was increased to 0.8
in order to maintain SaO2 above 97%. The physiotherapist obtained a sample of foul sputum for
culture and antibiotics were prescribed for pneumonia. A CXR showed typical localised changes at the
right base. It is now 7 p.m. and the HDU nurse has called you because she is again tachypnoeic and
hypoxic despite the therapy above. Chest signs are unchanged but she is noticeably sweaty and
starting to look tired. She is not in pain and, on detailed review, there does not seem to be anything
else you can do to improve matters. Recent blood gases show that the PaCO2 has risen from 4 kPa
to 7.3 kPa over the last 10 h. The HDU nurse is experienced and worried that the patient might
suddenly tire and arrest. You accept her advice and ask for an urgent ICU review. The ICU consultant
is pleased that you called at this stage. CPAP on HDU is considered but the patient is hypercarbic
and it is decided to take her to ICU for intubation and ventilation.

LEARNING POINTS
use your routine ward rounds to monitor progress systematically but re-assess and hand
over patients who are not right at the end of the routine day
detect patients who are failing to respond or deteriorating despite reasonable therapy and
refer promptly
clinical signs (e.g. tiredness and sweating) are also important in detecting the patient at risk
of respiratory failure and arrest.

43
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

The clinical signs and blood gas analysis are rate and tidal volume, be in control of his or her
the most important factors. Tachypnoeic patients own airway and able to co-operate. Patients who
suddenly tire and arrest. You must intervene fail to tolerate CPAP are recognised by refractory
before this stage by acting on early symptoms hypoxaemia, increasing respiratory rate and
and signs, particularly tachypnoea. Transfer the progressively smaller tidal volumes with subsequent
patient to a higher level of care for further therapy CO2 retention.
to improve gas exchange. An arterial line should Patient selection is key to the success of CPAP.
be inserted if frequent blood gas analysis is to be Frequent monitoring of the clinical status of the
performed. Anticipate problems in patients with patient is required, including regular ABGs, within
severe chronic lung disease (e.g. vital capacity less an HDU environment. A plan should be made of
than 15 ml/kg or FEV1 less than 10 ml/kg) and how frequently CPAP is to be used and for what
monitor them closely. length of time. Generally, to be beneficial,
a minimum of 2 hours of continuous CPAP is
CONTINUOUS POSITIVE AIRWAY PRESSURE required. CPAP may also be used as part of the
If the primary problem is Type I respiratory weaning process from formal ventilation or,
failure, CPAP by mask may help. A high flow alternatively, used post-extubation if the patient
source of oxygen-enriched air is supplied through has a high risk of re-intubation.
a tight-fitting facemask with a range of expiratory
valves (Fig. 4.5). These valves maintain a set
airway pressure, which can range from 2.510
cmH2 O. During ventilation, airway pressure
cannot drop below the pressure indicated on the
valve. This leads to recruitment of underventilated
alveolae, increases FRC, decreases intrapulmonary
shunt and may improve oxygenation.
The masks are uncomfortable to wear, may cause
nasal pressure sores and, if air-swallowing occurs,
result in gastric dilatation and regurgitation.
Some patients unable to tolerate a full-face mask
may tolerate a nasal mask but the patient must
keep their mouth closed to prevent loss of
pressure. CPAP may also be connected directly
via a T-piece to a pre-existing tracheostomy tube.
The patient must have a reasonable respiratory

Figure 4.5 Diagramtic representation of patient receiving

CPAP therapy.

44
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT
NON-INVASIVE VENTILATION BY MASK (BIPAP)
If Type II respiratory failure (CO2 retention)
develops, NIV support by mask should be
considered. Essentially, two different pressures
are applied to the patient via a facemask
a higher one during inspiration (around 20
cmH2 O) and a lower one in expiration (5 cmH2 O).
This may be termed BiLevel or BIPAP mask
ventilation. The pressure difference generates
gas flow into the lungs during inspiration.
The BIPAP machine detects inspiration by the
initial drop in airway pressure that occurs. It then
automatically raises the pressure to that set on
the machine for inspiration and changes back
to the lower level on expiration. The tidal volume
delivered is determined by the lung compliance,
duration of inspiration and the driving pressure.
This method of respiratory support may pre-empt
the requirement for intubation and ventilation and
requires critical care support. It is not effective in
all patients and, as with CPAP, careful selection
is required. It is not appropriate for patients who
are cardiovascularly unstable, who have decreased
level of consciousness, have a severe metabolic
acidosis or have poor respiratory rates. Patients
must be in control of their own airway and able
to co-operate. Patients who fail to tolerate mask
ventilation are recognised by refractory hypoxaemia,
increasing respiratory rate and progressively
smaller tidal volumes with worsening CO2
retention. In general terms, if the patients CO2
has not improved within 30 minutes, mask
ventilation is unlikely to succeed.
VENTILATION
Intubation and ventilation allows oxygen
concentrations of up to 100% and the volume
of each breath (tidal volume, Vt) and respiratory
45
rate or frequency (f) to be adjusted to suit the
patients needs. The minute volume (MV = Vt x f)
may be varied by altering the frequency or tidal
volume. The greater the MV, the greater the removal
of carbon dioxide, but too large a tidal volume
may cause barotrauma. Controlled mandatory
ventilation requires a fully sedated patient to
tolerate the presence of the tracheal tube and the
compulsory positive pressure breaths from the
ventilator. This mode of ventilation allows the
patient to play no part in breathing and is rarely
used. Most commonly, a synchronised intermittent
mandatory ventilation (SIMV) mode is used to
try and preserve some of the patients respiratory
muscle activity by synchronising ventilation
around the patients own respiratory efforts.
Escalation of respiratory PCIRV and
support via a ventilator high PEEP
PCV and
moderate PEEP
PSV and PEEP 5
CPAP or PEEP
only via ventilator
T-piece or TC
Increasing severity of respiratory failure
Figure 4.6 There are numerous modes of ventilatory support. The
balance needs to be reached between adequate gas exchange and
prevention of complications associated with artificial ventilation.
Ventilators are increasingly sophisticated and
offer different forms of ventilation, which may
be used in combination (Fig. 4.6). With modern
modes of ventilation, such as combining SIMV
with pressure control (PCV), pressure support
(PSV) and positive end expiratory pressure (PEEP),
there is much less need for sedation and paralysis.
Generally, only the most difficult patients to
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
ventilate should require paralysis and then only
for short periods until control is achieved.
With PEEP, pressure is administered during
expiration to prevent airway collapse and recruit
underventilated alveoli. Lung compliance, Vt
and how fast the Vt is pushed into the patient
determine the pressure reached within the airways
at the end of each breath from the ventilator.
This peak airway pressure can have adverse
consequences. The intrathoracic pressure is always
positive on inspiration during ventilation. This
causes decreased venous return and a fall in
cardiac output, which may be very severe if the
patient is hypovolaemic. PEEP can exacerbate this
problem. Furthermore, high values of peak airway
pressure and PEEP predispose to barotrauma,
which can result in tension pneumothorax.
High pressures plus high oxygen concentrations
may also promote the toxic effects of oxygen;
consequently, concentrations of oxygen greater
than 80% are rarely used and then only for the
shortest time possible. Peak airway pressures of
greater than 35 cmH2 O and the use of large tidal
volumes cause overdistension of alveoli and
damage to vascular endothelial tight junctions.
This process of volutrauma promotes alveoli
and vascular damage resulting in fluid leak and
worsening of lung compliance. This, in turn,
predisposes to even higher airway pressures.
Pressure control allows a breath to be administered
to a set pressure, kept below 35 cmH2 O; the tidal
volume then depends on the patients lung
compliance. By preventing high peak pressures,
the risk of barotrauma is reduced. With pressure
support, the ventilator senses that the patient has
taken an inspiration and administers pressure to
provide a higher tidal volume. The aim is not to
achieve a normal ABG but to provide adequate
46
ventilation without causing barotrauma. Usual
Vt is 1012 ml/kg but much lower volumes
(68 ml/kg) are used when ventilating. This leads
to a higher PaCO2 , termed permissive hypercapnia.
The CO2 is allowed to rise as long as the pH is
above 7.2. This reduces ventilator-induced lung
injury and is associated with improved survival
(termed lung protective ventilatory strategy),
though clearly, if lung compliance is very poor,
the CO2 may rise too high.
Lung recruitment strategies such as PEEP must
be combined with regular physiotherapy, suction
and turning the patient to prevent alveolar collapse.
CXR, ultrasonography or fibre-optic bronchoscopy
should be used to identify any lung collapse
amenable to bronchoscopic re-inflation, pleural
effusions or undiagnosed pneumothoraces.
Normally, the ventilator is set to provide less time
for inspiration than expiration. If the lungs are
very poorly compliant and stiff, the inspiratory
time may be increased to be equal or even longer
than the expiratory time. This process is known
as adjusting the inspiratory to expiratory (I:E)
ratio. The I:E ratio may thus be normal (1:2 or
1:3), equal (1:1) or inverse (2:1). Applying a
limited pressure for a prolonged period of time
aims to improve gas exchange by opening the
poorly compliant alveoli, holding them open for
as long as possible to maximise gas exchange
at pressures that will not cause barotrauma,
volutrauma or decrease cardiac output.
A patient on pressure controlled inverse ratio
ventilation (PCIRV), a high FiO2 of > 0.8, PEEP >
10 cmH2 O and permissive hypercarbia who fails
to achieve oxygen saturation of greater than 85%
is very likely to die. Death will occur from multiple
organ failure as tissue oxygen delivery fails to
meet demand. At this point, the use of an FiO2
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT
of 1.0 is justified and other adjuncts to ventilation
considered. The most commonly used is to turn
the patient from the supine to prone position.
Redistribution of blood flow to the less consolidated
or collapsed, more easily ventilated, anterior
portions of the lung may result in improved
oxygenation. Finally, ECLS with venovenous
cardiopulmonary bypass could be considered.
None of these adjuncts to oxygenation have been
shown to improve survival in prospective,
randomised, controlled trials in adults: survival
depends on adequate treatment of the underlying
cause of organ failure.
WEANING FROM VENTILATORY SUPPORT
Whatever the method of mechanical ventilatory
support used, if treatment of the underlying cause
of respiratory failure has been successful, then
the patient must be weaned from the ventilator
(i.e. returned to spontaneous respiration in a safe,
controlled manner). As soon as patients are able
to participate in ventilation, they should be
encouraged to do so as prolonged ventilation
will lead to atrophy of the respiratory muscles.
The various modes of ventilation can be used to
allow a gradual reduction in the amount of work
performed by the ventilator and an increase in
the respiratory effort of the patient.
In general, it is unwise to attempt weaning until:
the original cause of respiratory failure has
been treated successfully
sedative drugs have been reduced to a level
where they will not depress respiration
a low inspired oxygen concentration (40%)
maintains a normal PaO2
CO2 elimination is no longer a problem
sputum production is minimal
nutritional status, minerals, trace elements
are normal
47
neuromuscular function of the diaphragm
and intercostals is adequate
the patient is reasonably co-operative.
Most commonly used step-down modes are
SIMV, ASB or pressure support ventilation,
often again used in combination. Alternatively,
a simple T-piece may be used for periods of
time allowing the patient to do all the breathing
before being put back on mechanical ventilation
when they show objective signs of diminished
respiratory effort. The ventilator can be set to
simply compensate for the presence of the tube
(tube compensation, TC). The periods of time
spent breathing spontaneously are increased until
extubation is possible. In the majority of critical
care units, a combined approach is used with
PCV SIMV ASB/PSV CPAP and T-piece
followed by extubation. Patients may fail
extubation as a result of poor airway control,
laryngeal oedema, poor cough, sputum retention
or simple fatigue.
DISCHARGE FROM ICU
The period following ICU discharge is critical. In
particular, when transfer occurs to a general ward
without a period in HDU, the patient has to adapt
to reduced levels of nursing care, physiotherapy
and monitoring. A discharge summary and
suggested treatment plan will usually accompany
patients as they leave ICU but it is important
that this is understood by the ward staff and is
implemented directly. Experience shows that this
does not happen automatically! This period of
care exemplifies the importance of good personal
communication and organisation communication
between ICU and surgical staff, between surgical
and ward staff, of clear written instructions and
repeated assessment of the patient. Apart from
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
clinical re-assessment, ensure that medications
have been changed to ward format and started,
arrange out-of-hours physiotherapy as needed,
check the oxygen concentration needed and ensure
that any monitoring such as pulse oximetry is
available on the ward. Speak to the on-call team
and ask for formal review of the patient during
the evening. If the patient does deteriorate,
contact the ICU staff at an early stage; usually,
attention to the details of care and ensuring they
actually happen will prevent this.
COMMON SURGICAL
RESPIRATORY PROBLEMS
ATELECTASIS
Atelectasis is defined as an absence of gas from
all or part of the lung. It is commonly seen in
surgical patients, particularly following abdominal
and thoracic procedures. Reduced lung expansion
from pain and splinting leads to retention of
secretions and distal airway collapse. This is
exacerbated in the elderly, overweight, smokers
and those with pre-existing lung disease.
It should be anticipated in these patient groups
and prevented by pre-operative breathing exercises
to improve expansion, intra-operative care with
humidification, ensuring good tidal volumes and
avoiding unnecessarily high FiO2 . It can develop
rapidly, if unrecognised, into respiratory failure.
The symptoms of atelectasis are cough, chest pain
or breathing difficulty, low oxygen saturations,
pleural effusion (transudate) and cyanosis (late
sign) or tachycardia. Diagnosis is made by CXR.
Generally, the white cell count (WCC) and C-reactive
protein (CRP) levels remain in the normal range,
though it may rise with super-imposed pneumonia.
The mainstay of treatment is physiotherapy,
48
focusing on deep breathing, encouraging
coughing, and effective analgesia. An incentive
spirometer is often used as part of the breathing
exercises. Mobilisation should also be encouraged
to improve lung inflation. Some may benefit
from the use of CPAP. Antibiotics are given for
additional infection.
PNEUMONIA
Pneumonia is parenchymal or alveolar
inflammation and abnormal alveolar filling with
fluid (consolidation and exudation). In surgical
patients, pneumonia is usually bacterial or
chemical secondary to aspiration. Symptoms
include cough, chest pain, fever and difficulty
in breathing.
Physical examination of the lungs may be
normal but often shows decreased expansion of
the chest on the affected side, bronchial breathing
or crackles. Percussion may be dulled over the
affected lung. CXR, WCC, CRP and sputum and
blood cultures all help in diagnosis.
Hospital-acquired pneumonia is more likely to
be due to resistant bacteria such as MRSA,
Pseudomonas spp., Enterobacter spp. and Serratia
spp. Ventilator-associated pneumonia (VAP) is
a subset of hospital-acquired pneumonia and
occurs after 48 hours of mechanical ventilation.
Aspiration pneumonia is caused by aspirating
oral or gastric contents and may occur on induction
of anaesthesia. Material aspirated may contain
anaerobic bacteria leading to a secondary infective
pneumonia. Treatment depends upon the clinical
classification of pneumonia and also the known
bacterial resistances within each hospital. Local
microbiological advice should be sought.
 CHAPTER 4 | RESPIRATORY COMPROMISE IN THE SURGICAL PATIENT

Patients with pneumonia have a high risk of

developing respiratory failure and may trigger
ARDS, which results from a combination of
infection and inflammatory response. The lungs
quickly fill with fluid and become very stiff.
This stiffness, combined with severe difficulties
extracting oxygen due to the alveolar fluid,
creates a requirement for mechanical ventilation.
The CURB 65 score is frequently used when looking
at severity of pneumonia: Confusion; Urea > 7
mmol/l; Respiratory rate  30 per min; Blood
pressure (SBP < 90 mmHg or DBP  60 mmHg);
age  65 years. If three or more of these factors
are present, critical care admission is very likely
to be required.

PULMONARY EMBOLISM
Pulmonary embolism comprises embolic obstruction
of a vascular branch beyond the right ventricular
outflow tract, usually from an associated deep
vein thrombosis. They are still relatively common
in surgical practice, though thromboprophylactic
measures reduce the risk substantially.
Common symptoms include dyspnoea, pleuritic
chest pain, cough, haemoptysis and palpitations,
while signs include hypoxia, tachypnoea and
tachycardia. Diagnosis is based on these clinical
findings in combination with laboratory tests and
imaging studies. The gold standard for diagnosis
is pulmonary angiography but CT pulmonary
angiography is more commonly used (Fig. 4.7).
CXR may be helpful in excluding other causes
of deterioration. ABGs may show hypoxia and
hypocarbia. The most common ECG change,
apart from sinus tachycardia, is T-wave inversion
in the anterior leads and echocardiography may
be very useful in the unstable patient to look for
right heart dysfunction.
Figure 4.7 CTPA showing a saddle embolus and substantial
thrombus burden in the lobar branches of both main pulmonary
arteries.
TREATMENT
In most cases, anticoagulant therapy is the
mainstay of treatment. Usually, low molecular
weight heparin is administered initially, prior to
warfarin therapy. In the peri-operative patient,
treatment is complicated by the risk of bleeding.
If the risk of bleeding is high, unfractionated
heparin by infusion may be used with close
monitoring of APTT and monitoring of
cardiovascular status and haemoglobin may be
more appropriate. Alternatives include inferior
vena caval filter and pulmonary embolectomy.

49
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
If there is a concern regarding bleeding, heparin
can be stopped with its effect reversing within
3 hours; alternatively, it can be reversed with
protamine if a more immediate effect is required.
PRACTICAL SKILL: CHEST DRAINS
Chest drains are either inserted for pneumothorax
or for drainage of pleural fluid. There are two
main types of drain in common use. Seldinger-type
chest drains are most frequently used for drainage
of pleural effusions and small pneumothoraces,
while more traditional drains are inserted for
larger pneumothoraces (Fig. 4.8). The size of the
chest drain used depends on the indication: a
large bore tube (2830F) should be used for
haemothorax, large and/or tension pneumothorax
and a smaller calibre tube (1014F) for pleural
effusions. Maintenance of patency of chest drains
is important for safety; frequently, larger tubes
are inserted if there is any doubt. However, larger
chest drains are associated with increased pain.
Figure 4.8 Chest X-ray showing chest drain in area of partially
resolved R-sided pneumothorax.
50
The technique of chest drain insertion is not
taught on the CCrISP course. However, surgical
trainees should be able to recognise the indications,
methods and complications associated with chest
drainage.
All chest drains should be monitored for
swinging, draining and bubbling. Chest drains
should be removed as soon as they are no longer
required, i.e. a pleural effusion drained to dryness
(remember about 100150 ml of pleural fluid is
normally produced per day) or the pneumothorax
is fully inflated. Caution must be used when
patients are ventilated (including CPAP and
NIV) as re-accumulation of pneumothorax is
common and these may well be tension
pneumothoraces. If a patient has a pneumothorax,
generally any central line required should be put
in that side to prevent the occurrence of bilateral
pneumothorax. Chest drains should never
be clamped.
SUMMARY
assess respiratory function in all ward
patients who have undergone major surgery
and use simple measures liberally to prevent
major respiratory compromise
routine assessment is predominantly clinical
and aims to identify the patient who is
deteriorating
use the system of assessment to identify
clinically those patients with respiratory failure
instigate the level of treatment appropriate to
the severity of failure
treat the cause of the failure as well as
hypoxia/hypercarbia
re-assess clinical signs, oximetry and, most
importantly, ABGs
arrange safe transfer to higher level of care
for those who do not respond.
5
Arterial blood
gases and
acidbase balance

51
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the rationale for blood
gas analysis
interpret the results of blood gas analysis
in the surgical patient
understand how to manage acid base
disturbance within the CCrISP system of
assessment.
INTRODUCTION
ABG measurements are important in the
management of critically ill surgical patients
as they can provide a guide to acidbase status,
ventilation and global tissue perfusion, plus
potential compensatory mechanisms. Acidbase
status is expressed via pH, ventilation through
the partial pressures of oxygen and carbon
dioxide and tissue perfusion via base-excess/
base-deficit. Examining the trends of thesevalues
in the critically ill allows clinicians to analyse the
severity of a deterioration or effectiveness of their
management plans. Abnormalities in ABGs may
arise before a patient becomes obviously unwell
and thus provide clinicians with the opportunity
for early, effective intervention.
52
ABG samples are obtained by either arterial
puncture (usually the radial artery) or from an
arterial line (a-line; see Chapter 8). The complication
rates of such a procedure are low but include
bleeding and haematoma formation (particularly
in coagulopathic patients), distal ischaemia and
pseudo-aneurysm formation (the latter usually as
a consequence of infected in-dwelling catheters).
The techniques, risks and complications of
intravascular line placement are discussed in
Chapter 8. With respect to radial artery puncture,
the use of Allens test to demonstrate flow
through the ulnar artery theoretically ensures that
ischaemic damage will not occur due to collateral
circulation; in practice, for radial blood gas
sampling it is rarely used and the incidence of
digital ischaemia is low.
The arterial partial pressure of oxygen (PaO2) is
a reflection of the amount of oxygen dissolved
in the blood. Its relationship with the oxygen
saturation of haemoglobin (SaO2) is affected by
factors such as temperature, partial pressure of
carbon dioxide (PaCO2) and pH, which is reflected
by the oxygen dissociation curve (Fig. 5.1). The
PaO2 can be used as an indicator of the pressure
gradient that has the potential to drive oxygen
into the tissues. A normal (or supra-normal)
value does not necessarily ensure effective oxygen
utilisation by tissue but it does reflect adequate
management of oxygen delivery by the respiratory
and cardiovascular systems.

Regardless of what other ABG values show,
hypoxia should be treated with oxygen therapy.
A small group of patients with severe COPD rely
on hypoxaemia to drive their ventilation, and
high inspired oxygen concentrations (FiO2)
may suppress ventilation and cause hypercapnia.
However, clinical progress and serial ABG
measurement can assist in the management
of these patients; trainees should always seek
appropriate advice and help if unsure about the
potential for causing hypercapnia.
PRACTICE POINT
While hypercapnia can kill slowly, hypoxaemia
will kill quickly! Additionally, when interpreting
the PaO2, the FiO2 should be noted and
clinicians should always be aware of relative
hypoxaemia, i.e. an absolute PaO2 may be
within normal limits (1014 kPa) but the
amount of supplementary oxygen and ventilatory
support may be high. A more effective means
of assessing for relative hypoxaemia is the
PaO2:FiO2 ratio, whereby a ratio of < 40 kPa
is deemed hypoxic. Remember that, as the
FiO2 increases towards 1.0, the PaO2 should
increase an oxygen saturation of 100%
and PaO2 of 13 kPa indicates good oxygenation
for an individual breathing air (FiO2 0.21,
PaO2:FiO2 ratio 61.9 kPa) but not necessarily
for a patient on high flow oxygen (ratio 13
if the FiO2 is 100%). Note also that pulse
oximetry does not measure CO2 and, therefore,
reflects effective oxygenation rather than
effective ventilation; ABGs provide a better
overall picture of the ventilatory process
(see below).
53
CHAPTER 5 | ARTERIAL BLOOD GASES AND ACIDBASE BALANCE
100
90
80
70
60
SaO2 (%)
50
40
30
20
10
0
0 1 2 3 4 5 6 7 8 9 10 11 12 13
PaO2 (kPa)
Figure 5.1 The oxygen dissociation curve.
Metabolic activity in body tissue produces energy
(heat), carbon dioxide and acid, which reduces
the affinity of oxygen for haemoglobin; thus,
for a given PaO2, oxygen is less tightly bound to
haemoglobin enhancing its off-loading into cells.
As this occurs, 2,3-diphosphoglycerate (2,3-DPG)
present in red blood cells further loosens the bonds
between haemoglobin and oxygen. The reverse
is the case in the lungs, resulting in increased
binding between haemoglobin and oxygen.
INTERPRETING AN
ARTERIAL BLOOD GAS
A simple sequential approach to interpreting
ABGs can allow a doctor to detect abnormalities,
basic pathophysiological processes (metabolic
versus respiratory) and compensatory mechanisms
of any acidbase disturbance. Approximate normal
ranges for ABG components are outlined overleaf.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

NORMAL RANGES FOR ABG COMPONENTS

pH: normal range 7.357.45. Outlines whether a pathophysiological process has created an
acidaemia or alkalaemia.
PaCO2: normal range 4.55.5 kPa. This provides information about the absolute ventilatory
state of a patient and possible respiratory compensatory mechanisms.
HCO3: normal range 2428 mmol/l. Bicarbonate is the main plasma buffer; a low value
suggests consumption often due to increase acid-load (invariably lactic acid) and a high value
suggests retention of base to compensate for hypoventilation causing an acidaemia (see below).
Base deficit/base excess: normal range +2 to 2 mmol/l. This describes whether the bodys
buffers are being consumed (deficit) or retained (excess).
PaO2: normal range 1014 kPa. Outlines the level of oxygenation (taking into account the FiO2 ).
Serum lactate: normal range < 1.2 mmol/l. This is primarily a reflection of the extent of
anaerobic metabolism occurring within the body and secondarily a reflection of the livers ability
to metabolise lactate and regenerate bicarbonate anions.
The anion gap: normal range 1015 mmol/l. Plasma exists in electrochemical neutrality, i.e.
the number of cations and anions balance; however, the majority of laboratory assays measure
approximately 95% of cations and 85% of anions creating a differential described as the anion
gap or AG.
AG = ([Na+] + [K+]) ([Cl] + [HCO3])
The majority of unmeasured anions are plasma proteins but also include small concentrations
of phosphate, sulphate and organic acids. An acidaemia with an increase in the anion gap
indicates an increase in the concentration of these unmeasured anions (e.g. lactate and ketones).
An acidaemia with a normal anion gap equates to the total concentration of measured anions
being unchanged usually as a consequence of hyperchloraemic acidaemia. This is most frequently
seen following vigorous resuscitation with 0.9% saline but is also associated with bladder surgery
and ileal conduit formation.

54

ACIDBASE BALANCE
The concentration of hydrogen ions within the
body is normally tightly controlled at 40 nmol/l,
which is 7.42 pH units (pH = log10[H+]).
Over 1000 mmol of hydrogen ion is produced
per day, primarily as a result of the production
of carbon dioxide. This is excreted by the lung
and is dependent upon the minute ventilation
as controlled by chemoreceptors in the medulla.
There is also a smaller quantity of hydrogen ion
produced as non-volatile acid products of
metabolism of non-carbohydrate substrate, such
as phosphates and sulphates. This amounts to
approximately 1 mmol H+/kg/day and must be
excreted by the distal nephron. There are, therefore,
two control mechanisms maintaining hydrogen
ion homeostasis respiratory and renal.
The respiratory mechanism is a rapid-response
system that requires normal CNS function (central
pH chemoreceptors) and lung function to allow
carbon dioxide to be transferred from pulmonary
venous blood to alveolar gas and excreted in
expired gas. Any dysfunction of the mechanics
or control of respiration will cause retention of
CO2 and a rise in hydrogen ion concentration
(respiratory acidosis) or over-excretion and a
fall in hydrogen ion concentration (respiratory
alkalosis).
The renal mechanism is a slower responding
system that depends upon the excretion of hydrogen
ions in the urine by the distal nephron. Conditions
that impair renal function and, in particular,
distal nephron function (e.g. obstructive uropathy,
circulating volume depletion) will prevent non-
volatile hydrogen ion excretion resulting in a
metabolic acidosis.
55
CHAPTER 5 | ARTERIAL BLOOD GASES AND ACIDBASE BALANCE
The bodys homeostatic mechanisms with regard
to the maintenance of acidbase balance are
powerful and a patient can have a normal pH
in the face of marked physiological disturbance.
Furthermore, as the pH scale is a log-based scale,
small changes in pH represent major physiological
disturbances. Proteins are the primary buffer of
retained hydrogen ion; however, because of the
importance of the carbon dioxide/bicarbonate
system in the elimination of hydrogen ion, the
acidbase status of the body is best reflected by
the measurement of carbon dioxide tension and
bicarbonate level in the blood. This measures both
the volatile and non-volatile arms of the system.
(H+) + HCO3
H2CO3
H2O + CO2
Non-volatile Volatile
(Renal) (Respiratory)
RESPIRATORY ACIDOSIS
The retention of carbon dioxide will cause
a rise of H+ by driving the acid-base equation
to the left. The kidney will respond slowly
over approximately 48 hours to compensate
by increasing H+ excretion in the distal nephron,
thus returning H+ concentration toward, but
not completely, normal.
METABOLIC ACIDOSIS
The inability of the kidney to excrete non-volatile
hydrogen ion or a sudden increase in non-volatile
acid load (such as in sepsis) will drive the equation
to the right and respiratory function will rapidly
respond by increasing minute volume, reduce CO2
and cause hydrogen ion to return toward normal.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
RESPIRATORY ALKALOSIS
Respiratory alkalosis is caused by the minute
ventilation being higher than that required to
maintain the PaCO2 appropriate for a hydrogen
ion concentration of 40 nmol/l. The PaCO2 is
driven down and the hydrogen ion falls (pH rises).
This is usually caused by an increased central
respiratory drive commonly by fever, hepatic
disease, aspirin toxicity or CNS dysfunction.
METABOLIC ALKALOSIS
Metabolic alkalosis occurs when the level of
bicarbonate in the blood is increased due either
to abnormal retention or administration of
bicarbonate or the loss of non-volatile acid from
the body (gastric outlet obstruction or chronic
nasogastric aspiration). Abnormal retention of
bicarbonate can occur in association with chloride
depletion due to loop diuretics and is also seen
in chronic hypokalaemia.
Knowing the hydrogen ion concentration/pH,
PaCO2 and bicarbonate allows the acidbase status
to be determined, thus the type of abnormality
and degree of compensation to be estimated.
The most useful bicarbonate measure is the
standardised value, which corrects the measured
bicarbonate to the value that would be present if
the PaCO2 was normal (40 mmHg or 5.4 kPa). The
non-volatile acidbase state is also summarised
by the calculated base excess, which gives a
value of the difference between the standardised
bicarbonate and the normal value. This is otherwise
considered as the amount of acid or alkali needed
to return blood in vivo to normal pH under
standard conditions.
56
THE MANAGEMENT
OF ACID-BASE DISTURBANCE
The first step is to manage the patient according
to CCrISP principles and then investigate the
nature of the disturbance using ABG samples and
other investigations relevant to the patients history.
The importance of determining the underlying
primary disturbance can point the clinician
towards definitive treatment of an underlying
problem. While this is achieved, measures may
be required for temporary correction of the pH
by other means. Examples of aetiologies and case
histories are illustrated below:
AETIOLOGY OF COMMON
ACID-BASE DISTURBANCES
Metabolic acidosis
impaired tissue perfusion deal with cause,
improve circulation/perfusion
renal failure deal with cause, bicarbonate,
renal replacement therapy
hepatic failure ?transplant.
Respiratory acidosis
head or spinal injury ventilation
drug overdose antidote (e.g. Naloxone)
and/or ventilation if indicated
chest wall deformity or injury ventilation
if indicated
myopathy or peripheral neuropathy
ventilation if indicated
pulmonary disease treat disease, respiratory
support and ventilation if indicated
massive pulmonary embolus re-establish
perfusion of ventilated lung.

EXAMPLES OF ACIDBASE DISTURBANCE
IN CLINICAL PRACTICE
CASE 1
A 54-year-old man, 14 h post-laparoscopic
hemicolectomy, receiving oxygen at 4 l/min
via a facemask and using a morphine PCA.
Respiratory rate is 8 breaths/min.
ABGs:
pH, 7.24
PaCO2 , 9.8 kPa
PaO2 , 15.1 kPa
HCO3 , 24.2 mmol/l
BE, +0.2 mmol/l
Lactate, 0.9 mmol/l
What is the nature of the blood gas abnormality
and how should you manage the situation?
This is an uncompensated respiratory acidaemia,
most probably caused by excess opiate.
Oxygenation remains good; however, in time,
the patient will become hypoxaemic without
intervention. Assess using the CCrISP system
with early administration of high flow oxygen
and Naloxone.
57
CHAPTER 5 | ARTERIAL BLOOD GASES AND ACIDBASE BALANCE
CASE 2
A 72-year-old woman with known diverticular
disease presented to the surgical admissions unit
with abdominal pain and peritonism. Respiratory
rate is 28 breaths/min and breathing face mask
oxygen at 4 l/min.
ABGs:
pH, 7.30
PaCO2 , 3.8kPa
PaO2 , 9.1 kPa
HCO3 , 18.7 mmol/l
BE, 7.0 mmol/l
Lactate, 2.1 mmol/l
What is the nature of the blood gas abnormality
and how should you manage the situation?
This patient has a partially compensated metabolic
acidaemia and is hypoxic. She is likely to have
intra-abdominal sepsis with increase acid load
indicated by loss of buffer (low HCO3 ) and raised
serum lactate. The tachypnoea is a consequence
of an attempted compensation for the acidaemia
and also the likely consequence of pain, which in
turn can cause diaphragmatic splinting, atelectasis,
hypoxaemia and, if ineffectively managed,
worsening hypercapnia. This patient requires
aggressive resuscitation, analgesia and management
of the source of sepsis (source control).
PRACTICE POINT
Be aware of the tachypnoeic, acidaemic
patient with a raised CO2 .
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
CASE 3
A 48-year-old man with Crohns disease,
an ileostomy and large stoma losses. He is
tachypnoeic and breathing room air.
ABGs:
pH, 7.25
PaCO2 , 3.2kPa
PaO2 , 17.1 kPa
HCO3 , 14.2 mmol/l
BE, 9.9 mmol/l
Lactate, 1.0 mmol/l
What is the nature of the blood gas abnormality
and how should you manage the situation?
He has a metabolic acidaemia with attempts at
compensation but not effective enough to prevent
a low pH. There is likely to have been large loss
of bicarbonate from the stoma. In addition to
CCrISP assessment, investigation and treatment
of the cause, fluid replacement with a crystalloid
such as Hartmanns solution is appropriate to replace
many of the electrolytes being lost; furthermore,
if the liver function is normal, the lactate anions
can be utilised to generate bicarbonate, help
replace losses and correct the acidaemia.
58
CASE 4
A 78-year-old man presents to surgical
admissions 1 month after a Whipples procedure
with nausea and vomiting for the previous
3 days, and a distended abdomen.
ABGs:
pH, 7.54
PaCO2 , 6.7 kPa
PaO2 , 11.5 kPa
HCO3 , 31.5 mmol/l
BE, +4.8 mmol/l
Lactate, 0.7 mmol/l
What is the nature of the blood gas abnormality?
He has a partially compensated metabolic
alkalaemia, most probably secondary to loss of
gastric acid through vomiting, quite possibly
induced by gastric outlet obstruction.
SUMMARY
The interpretation of blood gases is an essential
part of caring for surgical patients.
pH indicates whether there is acidosis
or alkalosis
base excess indicates whether acidosis is
metabolic (negative base excess) or respiratory
low PaO2 indicates the presence of hypoxia
high PaCO2 and acidosis (plus high HCO3
and positive base excess) indicates respiratory
acidosis
initial management of any acidbase
disturbance begins with the CCrISP algorithm.
6
Cardiovascular
disorders,
diagnosis and
management

59
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
After reading and understanding this section
you should be able to:
assess your patient to determine whether
the cardiovascular system is functioning
adequately
determine if the problem is primarily
cardiovascular in origin
determine the most likely underlying
pathology
decide where and how this should be
appropriately treated
initiate safe and appropriate management
of common cardiac pathologies.
The following three chapters deal with aspects
of cardiovascular disorders, shock and monitoring
and should be considered together. This first
section will introduce a basic pattern of thinking
that should enable the early detection of an
impending cardiovascular problem. Preventative
measures, simple treatments or referral to a
specialist unit can then be initiated appropriately.
This chapter will focus on clinical assessment
and the diagnosis and management of cardiac
disorders. Management and treatment of shock
will be covered in Chapter 7, while more invasive
monitoring and support will be detailed in
Chapter 8.
Disorders of the CVS are very common in the
sick surgical patient and can be due to associated
medical co-morbidity or arise as complications
following surgical procedures. Despite the presence
of an intact airway and adequate ventilation, any
problem causing decreased efficiency of the CVS
60
can result in inadequate delivery of oxygen to the
tissues for their metabolic needs. This will initiate
a cascade of adverse events that will lead to the
development of organ failure. The range of
pathologies that cause CVS disturbance is broad,
including inadequate or excessive circulating
volume, primary pump problems and increased
or reduced afterload. While organ failure may be
obvious, it more frequently presents with more
subtle and gradual deteriorations in the presence
of apparently normal or slightly deranged pulse
rates and blood pressure. Early recognition of an
impending problem and initiation of effective
treatment will increase your patients chances of
survival and help to prevent further complications.
Prediction and prevention are vital.
For these reasons, the approach to the examination
of the CVS must be systematic, accurately
documented and repeated frequently. The effect of
any intervention, such as fluid administration, must
be re-assessed to ensure its efficacy and durability.
It is also imperative to pay great attention to a
patients concurrent cardiac medications.
PATIENT ASSESSMENT
AND MANAGEMENT
IMMEDIATE ASSESSMENT AND RESUSCITATION
To establish that the patient does not need
immediate life-saving resuscitation, you need to
make your immediate ABC assessment using the
CCrISP algorithm. Keep an open mind; do not try
and make the findings fit any preconceived
diagnosis, and remember to initiate immediate and
appropriate resuscitation during the assessment.
Hypovolaemia due to haemorrhage or unreplaced
fluid losses should be considered the primary
cause of CVS dysfunction in the surgical patient
until proved otherwise. Thereafter, sepsis, cardiac
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT
dysfunction or pulmonary embolism represent
common problems.
The presence of dyspnoea increases the likelihood
of a cardiac and/or respiratory problem. Breathing
and the CVS are inextricably linked; a disorder of
the respiratory system (e.g. tension pneumothorax)
may produce CVS signs and similarly a CVS
disorder (e.g. left ventricular failure) may produce
respiratory signs.
All other organ systems are dependent on the
viability of the circulation. This is particularly
true of the renal and the central nervous systems,
and the integrity of these end organs can give
valuable information about the function of the
CVS. If the patient is obtunded or too confused to
respond coherently, then cerebral hypoperfusion
or hypoxia is likely and prompt action will
be needed.
Life-threatening CVS disorders are recognisable
if you examine the patient appropriately:
look for: pallor, poor peripheral perfusion,
underfilled or overfilled veins, obvious blood
loss from wounds, drains or stomas, swelling
of soft tissues or other evidence of concealed
haemorrhage into chest, abdomen or pelvis.
Ankle or sacral oedema
listen to the patient: confusion might be due
to poor cerebral perfusion; if they say they
feel faint on sitting up or are thirsty, consider
hypovolaemia. A complaint of breathlessness
on lying flat may point to fluid overload.
Complaints of chest pain, breathlessness,
feeling feverish or cold are all helpful in
determining underlying pathology and should
not be ignored. Listen to the chest and heart.
61
PRACTICE POINT
Listen to the heart normal heart sounds
or gallop rhythm?
Is there a new murmur?
feel for: carotid and femoral pulses if peripheral
radial pulses are not present. Assess for rate,
quality (weak/thready/strong), regularity and
equality. Examine for swelling, distension or
painful areas that may indicate internal bleeding
or ischaemia. Feel for changes in skin
temperature and assess capillary refill.
PRACTICE POINT
Unwell surgical patients will benefit from
oxygen and fluid therapy while you are
performing your assessment.
FULL PATIENT ASSESSMENT
Chart review
The notes and charts contain a lot of data; again,
a systematic approach minimises the chance of
missing important facts. Sometimes, it can be
useful to complete your note and chart review
before speaking in detail to the ward nurses and
doctors. This provides you with a factual base for
discussing the patient in more detail. The notes
will provide basic clinical information on pre-
morbid status, co-morbidity and any procedures
performed. On the charts, look at both the
absolute values and the trends. Absolute values
are notoriously unreliable and more useful
information can be obtained by looking at trends
over the preceding few hours. The charts should
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
indicate the progress of the patient and important
parameters include:
respiratory rate, oxygen FiO2 and saturation
heart rate and rhythm
blood pressure systolic/diastolic
CVP (if measured)
temperature
urinary output
i.v. lines position and condition
fluid therapy prescribed versus given,
drainage of all types
review drug chart for drugs with CVS effects
(given/omitted).
Respiratory rate
most sensitive marker of the ill patient
and often the first parameter to change as
the patient deteriorates
accurate observation and recording is essential
rates < 11 may be due to opiate/sedative
overdose or other causes of CNS depression
including low cardiac output
high respiratory rate is an early sign of many
kinds of shock, as well as respiratory disease
or cardiac failure
an increased respiratory rate may be in
response to hypoxia and/or metabolic acidosis.
Heart rate and rhythm
there is wide individual variation with age
and disease
interpret absolute values of pulse rate along
with co-existing medical conditions or drug
treatment: beware the patient on -blockers
or who has a pacemaker as the normal cardiac
response to hypovolaemia or pyrexia will
be blocked
tachycardia can be an early sign of shock
acute dysrhythmia is an important sign of
myocardial failure or ischaemia.
62
Blood pressure
changes in both systolic and diastolic pressure
are often late signs but, when present, should
flag up the severity of the underlying problem
think perfusion rather than pressure: a high
or normal blood pressure with poor perfusion
is of little benefit to the patient
remember that for the elderly patient who
usually runs at 180/100, a pressure of 110/70
represents significant hypotension.
Clinical signs may be unreliable in that normal
values do not exclude significant abnormality.
However, abnormal values should be acted upon!
Jugular venous pressure/central venous pressure
jugular venous distension measured with
the patient 45 in the sitting position will give
a clinical indication of the CVP
collapsed neck veins with the patient at 45
indicates low JVP
JVP not visible with the patient flat is
always abnormal
the CVP response to a fluid bolus is a better
guide to fluid status than absolute value
the trend in CVP reading is a very valuable
tool in assessing ongoing fluid status
consider formal CVP monitoring early in
ill patients when management of fluids is
becoming problematic.
Abnormalities relating to the CVP are detailed
in Table 6.1.
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT
TABLE 6.1
ABNORMALITIES OF CVP
A low CVP may be:
due to inadequate fluid therapy
an indication of continued bleeding
due to vasodilatation in response to sepsis
may be associated with a low cardiac
output
explained by vasodilatation due to
epidural analgesia exclude other causes!
a low CVP must be corrected in the face
of hypotension.
A high CVP may be:
temporary following a rapid fluid bolus
a result of fluid overload
due to right ventricular failure as a result
of MI or pulmonary embolism
due to CCF
due to chronic respiratory disease
caused by pericardial effusion with
tamponade.
If in any doubt as to the cause or treatment
required, seek expert help!
Temperature
may be high (> 38C) or low (< 36C) in sepsis
or SIRS but may be normal even in the
presence of severe intra-abdominal sepsis in
the immunocompromised, elderly or patient
on steroids
core/peripheral temperature (rectal/axillary)
difference > 2C suggests poor peripheral
perfusion
63
low-grade pyrexia occurs after MI in bacterial
endocarditis (irregular, mild and accompanied
by a cardiac murmur and anaemia) or with
diurnal variation in a warm environment (highest
in the early evening).
Urinary output
probably the best surrogate marker of cardiac
output and tissue perfusion that is readily
available on the ward BUT it is not an
immediate and acute measurement
the hypoxic or underperfused kidney does
not perform well and is an excellent marker
of early cardiovascular problems
look for a steady decline to indicate a problem
rather than sudden complete anuria, which
suggests a blocked catheter.
Intravenous lines
careful aseptic management of i.v. lines is
essential to avoid line sepsis
Large-bore i.v. access is required to deliver
an appropriate rapid fluid bolus
tissued lines cause morbidity both from the
local effect of extravasated fluids and drugs
and, systemically, as a result of the failure
of the fluid and drugs to reach the circulation.
A patient with a tissued drip relying on i.v.
fluids may become dehydrated quickly.
Tubes and drains
may or may not be patent
sudden occlusion of chest drains may lead to
tension pneumothorax
pericardial drains occluding after cardiac
surgery may cause cardiac tamponade
occluded abdominal drains may delay
recognition of ongoing bleeding
drainage volumes and nasogastric aspirate are
an essential part of fluid balance calculations.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Drug chart review
may reveal that regular cardiac drugs have been
omitted while the patient was nil-by-mouth
alternatively, drugs may have been
administered that have produced adverse
cardiovascular effects as a result of overdosage,
accumulation or interaction with other systems
(e.g. steroids preventing pyrexia in sepsis or
masking abdominal signs).
Fluid balance
determine type and quantity of fluids given;
the fluid balance for the current 24 hours and
for the preceding days
has the fluid been given as prescribed (often
inadequate, slow or curtailed)?
it is much more frequent for unwell surgical
patients to be hypovolaemic rather than fluid
overloaded
however, pulmonary oedema may be iatrogenic,
particularly in the elderly patient with a
cardiac history. In these patients, fluid should
be given in small repeated boluses to correct
hypovolaemia
remember that all patients are different and
do not respond identically to apparently similar
fluid regimens.
History
Taking a careful and detailed history from the
patient and from the notes will help to identify
cardiac problems. Remember that nursing
colleagues and relatives can be useful additional
sources of information. Specific points worth
remembering include:
speed of onset and duration of any symptoms
pain, its nature, severity, site and radiations
presence of dyspnoea
functional exercise tolerance.
64
Case notes
The pre-admission cardiac status and medication
should be identified from the notes when making
an assessment of the CVS, both when complications
are occurring and when the daily management
plan is being formulated.
Examination
Utilise all the available clinical information and
think perfusion. Concentrate on the CVS.
LOOK
overview is the patient alert? A reduced
level of consciousness is often a clear sign
of reduced cardiac output
colour presence of peripheral or central
cyanosis; anaemia
peripheries assess for peripheral perfusion
and presence of oedema. Assess limb
temperature
neck veins.
LISTEN
Breath sounds
assess for the presence of basal crepitations,
indicative of left-sided failure
in early, left-sided failure, bronchial
wheeze (cardiac asthma) may be present
due to small airway narrowing as a result
of interstitial pulmonary oedema.
Heart sounds
assess for the presence of added sounds
or murmurs (?new)
time the murmur with the carotid pulse:
remember a diastolic murmur is never
physiological.
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT
FEEL
skin may feel clammy with poor capillary
filling in cardiogenic shock or warm with
good capillary refill in sepsis
liver assess for presence of hepatomegaly
or ascites which may be an indication of
congestive heart failure. Heart failure can
cause abdominal pain from acute distension
of the liver capsule.
TABLE 6.2
INDICATORS OF A LOW CARDIAC OUTPUT
Cool, clammy skin with poor capillary
flushing
Rapid, low volume pulse
Peripheral cyanosis
Low peripheral temperature/core: peripheral
temperature gradient (> 2C)
Oliguria or anuria
Confusion
Metabolic acidaemia.
Available results
Include the available results and previous
investigations in your assessment. Remember that
ward care is different to HDU/ICU care and it is
unlikely that the complete range of cardiovascular
tests will have been performed. Be realistic, look
at what is available and use the findings of your
clinical examination, note and chart review to
determine if any further specific tests are required.
Demanding unnecessary tests is time consuming,
65
costly and inflicts further discomfort to the patient.
As a minimum to aid your assessment, look at
the most recent haemoglobin, white cell count,
platelet count and electrolyte/urea and compare
them with those taken when the patient was well.
If no contemporary results are available since
deterioration, these will need to be ordered.
Additional tests will be necessary if you suspect
particular problems (e.g. cardiac enzymes for MI).
Blood results
Haemoglobin
anaemia may well precipitate failure in the
cardiac patient and caution will be required
during transfusion. Diuretic cover may be
needed (but not always consider cardiac
function and volume state)
recent studies show that transfusions should
be used to maintain a haemoglobin level
around 8 g/dl
if the patient is actively bleeding, more blood
will be required.
Electrolytes
potassium and magnesium are particularly
important for cardiac function (see Chapter 11)
if infarction/ischaemia is suspected, serial
troponin levels should be measured from 6
hours after the onset of symptoms
brain natriuretic peptide (BNP) levels may
help in assessing heart failure.
The chest X-ray
The chest radiograph can help differentiate
respiratory conditions from cardiovascular and
aids in the positive identification of heart failure.
Refer to the system for looking at radiographs
in Chapter 4.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Remember chest X-rays take time and should dysrhythmias in surgical patients will be given
not delay treatment. If the patient is unwell, they during the practical course.
should not be sent to the radiology department
without monitoring and the appropriate level
of care. INTERPRETING THE ECG

The electrocardiograph OBJECTIVES

As with other investigations, the ECG should
never be looked at in isolation but should be
interpreted in light of the clinical findings. It
may show nothing significant, even in the failing
heart, but it is important to be able to recognise
common patterns. Most bedside monitors do
not show a trace adequate for accurate diagnosis
so a formal 12-lead ECG is essential. Further
instruction and practice in the interpretation
of ECGs and the management of common
to learn a system for examining ECGs
to be aware of the common important
abnormalities in critically ill surgical patients
to know the initial treatment of common
cardiac dysrhythmias.
Always work to a routine when looking at an
ECG (Table 6.3). Check patient name/date/time
and compare with previous ECGs.

TABLE 6.3

THE ROUTINE FOR LOOKING AT AN ECG

Axis Use deflection in bipolar leads
Rhythm Use the R wave (lead II) ?Regular
Rate Use the R wave ?Normal
P wave Presence and morphology ?Sinus rhythm
PR interval Short Pre-excitation (e.g. WPW)
Long (e.g. heart block)

QRS complex Height, width, presence Q waves ?MI, ?BBB

ST segment Depressed or elevated ?MI, ?ischaemia, ?digitalis toxicity
T wave Height, shape ?Ischaemia, ?biochemical abnormalities
U wave Presence ?Hypokalaemia

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 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

ROTATION OF THE HEART AND MORPHOLOGY

OF THE PRECORDIAL QRS COMPLEXES B

The rotation of the heart determines the appearance V1 V2 V3

V4
of the QRS complexes in the different leads a)
(Fig. 6.1). The size of the R wave in V1 increases
V5
progressively towards V6 because the underlying
myocardium becomes progressively thicker over
V6
the left ventricle. Note depolarisation occurs
from endocardium to epicardium and this reflects
myocardial thickness. Occasionally, the R wave
in V6 may be smaller than V5 and that in V5
may be smaller than V4 this is because the
electrodes in these leads are further away from A

Clo
ck
the myocardium than in V1 to V3 in these cases. b)

wi
V1 V2 V3

se
V4
The size of the S wave (first negative deflection
after the R wave) tends to decrease towards V6. A
V5
The direction of the first part of the QRS complex
B
is upwards in V1 to V3 (an R wave) but this
becomes a negative deflection as it progresses V6
to V6 (Q wave). This is not pathological and is
due to rotation of the heart about a near vertical
axis (left hip to right shoulder), thus producing
a variation in the relative positions of the two A
ventricles. This rotation causing the variations c)
V1 V2 V3
in QRS complexes is not clinically significant and
V4
is e

is dependent on the individual.

ck w
ic lo

Since the height of the R wave and depth of the

A nt

V5

S wave are influenced by the thickness of the

underlying myocardium, these deflections will V6

be abnormally large in conditions producing

hypertrophy, for example, left ventricular
hypertrophy secondary to hypertension or aortic
valve disease. However, in the thin individual the
R wave may be abnormally high over V4 to V6. B

Figure 6.1 Rotation of the heart and morphology of the

precordial QRS complexes. The cross section through the thorax
is viewed from below. (a) intermediate position, (b) clockwise
rotation, (c) anticlockwise rotation.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

THE ELECTRICAL AXIS OF THE HEART
The spread of depolarisation across the myocardium
produces vector loops of electrical activity.
When the depolarisation wave moves towards an
electrode, an upwards or positive deflection will
be recorded. Conversely, moving away from an
electrode will produce a downwards or negative
deflection. The angle at which this electrical wave
moves in relationship to a particular electrode
will determine the degree of upward or downward
deflection recorded by it. Each lead of the ECG
looks at the heart from a different aspect, or
angle. These angles can be displayed using the
Hexaxial Reference System.
Fig. 6.2 shows the angle that each bipolar lead
sees of the heart. By comparing the relative
heights of the R wave and depth of the S wave,
the electrical axis or sum of the depolarisation
vectors can be determined. Basically, the more
the electrical axis points towards an electrode, the
greater the deflection produced by that electrode.
See leads II and F in Fig. 6.2a and leads L and I
in Fig. 6.2b.
This description is simplified and is only intended
to give you an outline of the subject.

a)

R L L I

I
90 II F
120 60

150 30 III R
R L III II
F
180 I
0
+180
b)

+150 III II +30 R L

F
+120 +60
+90 I L I

II F

III R
III II
F

Figure 6.2 Electrical axis of the heart.

68
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

II

II

90
120 60

(aVR)150 30 (aVL)
R L
aVR

180 I
0(I)
+180

+150 III II +30

F
aVL
+120 +60
(III) +90 (II)
(aVF)

Figure 6.3 Example to demonstrate determining the electrical

axis of the heart.
aVF

Look at the example provided in Fig. 6.3.

Using the theory above, can you determine the
electrical axis?

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

TABLE 6.4

NORMAL ECG RANGES

At 25 mm/s Large square = 0.2 s

Small square = 0.04 s
QRS width Normal < 0.12 s
Wide > 0.12 s
Tachycardia Is a ventricular rate > 100 bpm
Bradycardia Is a ventricular rate < 60 bpm
Electrical axis +90 to 30
Vertical +60 to +90 (tall individuals)
Intermediate +30 to +60
Horizontal +30 to 30 (stocky, squat individuals)
Axis shifts towards the left in the elderly
T wave Normally upright, except in aVR. Inversion can also occur in III, V1 and V2
P wave Normally upright
Inversion can occur in retrograde P waves in AV nodal rhythm
Tall, peaked waves in pulmonary hypertension (pulmonary P)
Biphasic in mitral valve disease (mitral P)
PR interval Measured from the start of the P wave to the first deflection of the QRS
complex, whether it be upright to inverted
Range = 0.120.2 s
QT interval Variable, depends on rate
Q wave The first downward (negative) deflection after the P wave
Normal in lead III and aVR and sometimes in V4, V5, V6
Width no more than 0.04 s duration
Depth no more than one quarter the height of the following R wave
U wave Normal when T wave is normal, but in hypokalaemia it may become more
prominent as the T wave flattens

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 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

NORMAL RANGES IN ECG INTERPRETATION

The normal ranges in ECG interpretation are
shown in Table 6.4 and Figs. 6.4 and 6.5.

(mV) R Time

T I aVR V1 V4
P

Q
S

Wave P QRS T

Segment PQ ST II aVL V2 V5

0.12-0.2s c. 0.35s
Interval PQ QT
(frequency dependent)

Figure 6.4 Normal annotated PQRST.

III aVF V3 V6

DECIDE, PLAN AND TREAT

The clinical assessment and investigations
described above should lead to a diagnosis that
explains the patients deterioration. The next task
is to reach a decision based on the findings and,
if needs be, arrange appropriate investigations or
specialist opinions. Make a management plan to
treat the problem and prevent recurrence.
Conditions that do not rapidly resolve with
relatively simple measures will require expert help
and a higher level of care. After any intervention
you will need to re-assess and modify the
management plan.
Figure 6.5 Normal ECG trace.
Remember the CVS has considerable reserve and,
by the time dysfunction is evident, the problems
are marked. Do not leave patients with obviously
compromised cardiovascular systems they wont
be there when you get back!
SPECIFIC MANAGEMENT PROBLEMS
DIAGNOSIS AND MANAGEMENT
OF HYPOTENSION
Remember that hypotension is the commonest
cardiovascular problem seen in surgical critical
care patients. This has been discussed in the

71
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

chapter on patient assessment (Chapter 2) and MANAGEMENT ALGORITHM

will be explored further in the chapter on shock FOR TACHYARRYTHMIAS
(Chapter 7). Assessment
A systematic approach to the problem should be
DIAGNOSIS AND MANAGEMENT adopted, using the CCrISP algorithm.
OF TACHYARRYTHMIAS check and correct ABCs CPR or immediate
Being called to evaluate a surgical patient with anaesthetic and cardiology support may be
a tachycardia is common (Table 6.5). Management necessary. It is better to summon help before
initially follows the system of assessment. arrest occurs
A patient with unstable vital signs needs prompt 12-lead ECG to allow accurate diagnosis
diagnosis and treatment. At the other end of the and exclude MI
spectrum, long-standing, asymptomatic AF is rule out/correct: hypovolaemia, hypoxia,
common in the elderly and might simply need hypokalaemia; hypomagnesaemia
attention to fluid balance and re-institution of check routine medications have been given.
routine digoxin treatment. Usually, some action
will be required. If any doubt exists, ask for Autonomic manoeuvres
senior help. carotid sinus massage and Valsalva manoeuvres
may correct a supraventricular tachycardia as
TABLE 6.5 described below but this is unlikely to be
permanent.
CAUSES OF TACHYCARDIA
(The type of tachycardia will only be evident Drugs
from the ECG) care must be taken with all drugs, particularly
in patients with poor ventricular function or
Trauma Hypovolaemia, anaemia,
hypotension
contused myocardium
there are various groups of drugs available
Inflammatory Pyrexia, pericarditis for the treatment of tachyarrythmias
if the diagnosis is not clear after clinical
Metabolic Acidosis
and ECG interpretation, the administration
Haematological Anaemia of adenosine can be revealing (see below)
only use a drug if you are familiar with its
Circulatory Shock, from any cause,
actions and its side effects
arrhythmias, PE, MI
if there is any doubt about a drug, it should
Endocrine Thyrotoxicosis not be given and help must be sought early!
remember, in the longer term, if AF or flutter
Drugs Aminophylline, digitalis
persists, anticoagulation will be necessary in
toxicity, b-agonists
order to prevent emboli.
Anxiety and pain

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 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

CASE SCENARIO 6.1

A 73-year-old man, who is a known hypertensive who usually takes amlodipine, underwent anterior
resection for carcinoma of the rectum this morning. You review him at 8 p.m. on the evening of
surgery and find him to be in AF with a rate of 90 bpm. This developed about 30 min previously.
On your immediate assessment you find that he appears quite well and tells you that he feels
comfortable (he has an epidural infusion in progress). His respiratory rate is 18 breaths/min and
his oxygen saturation is reading 97% with facemask oxygen at 40%. You examine him and find
that his peripheries are well perfused. His blood pressure is unchanged from pre-operatively at
150/80. Your initial assessment reveals no other findings. You review his charts and notes and find
that his urine output has only been 40 ml over the last 2 h. His CVP has been gradually decreasing
since return from theatre and is now reading 2 mmHg. He was prescribed 2 units of blood to run
over 3 h each, followed by 1000 ml saline 8-hourly by the anaesthetist. The first litre of saline has
just been started. You ask the nurse to give him the litre of saline over 1 h, and check a full blood
count and his urea and electrolytes. His haemoglobin is satisfactory at 11.0 g/dl. His serum potassium
is 3.2 mmol/l. All other electrolytes, including magnesium are within normal limits. You prescribe
20 mmol of potassium to be given in 100 ml saline over the next hour and arrange with the sister
in charge of HDU to review him in an hour. When you review him, he is in sinus rhythm with a rate
of 75 bpm, his CVP has risen to 6 mmHg and he has passed 30 ml of urine over the past 30 min.
You change the fluid prescription to 1000 ml saline with 20 mmol KCl per litre 6-hourly and arrange
to review the patient again later that evening.

LEARNING POINTS
use the CCrISP system of assessment to review all patients
regular review of patients at risk will lead to early detection of potential problems
correction of hypovolaemia, hypoxia and electrolyte disturbances is simple but is often
very effective.

DC cardioversion Pacing and surgical ablation

should be considered early when very rapid The use of these treatments is beyond the scope
rate or evidence of compromise, particularly of this manual. These should be used as a last
for ventricular tachyarrythmias resort under the guidance of a cardiologist.
the patient must be anaesthetised
less effective in cases of long-standing atrial
arrhythmias
appropriate help must be sought at an early stage.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

TABLE 6.6

COMMON CAUSES OF ARRHYTHMIA

Ischaemic heart disease
Oxygen, fluid and electrolyte disturbances
Drugs Figure 6.6 Supraventricular tachycardia.
Rheumatic heart disease
Cardiomyopathy
Thyrotoxicosis Fusion beats

VENTRICULAR TACHYARRYTHMIAS
VENTRICULAR TACHYCARDIAS Figure 6.7 Ventricular tachycardia.
Even the most common arrythmias (Table 6.6)
may require cardiology input for safe and effective
management. Ventricular tachycardias (VT) are TABLE 6.7
potentially very serious and require prompt
specialist referral. They should be distinguished DIFFERENTIATING SVT AND VT
from SVT by the appearance of the ECG (Figs. Chamber of origin
6.6 and 6.7, Table 6.7). Cardioversion is often
required for VT and this is particularly urgent Supraventricular (SVT) Ventricular (VT)
if the patient has evidence of compromised QRS narrow complex Often broad complex
cardiac output.
Often no P waves P waves dissociated
SVT may respond, although sometimes only
rhythm
temporarily, to intense vagal stimulus created by
carotid sinus massage or the Valsalva manoeuvre. Usually regular May be irregular
Otherwise, adenosine can be administered (0.05
QRS right way up QRS inverted
0.25 mg/kg). It has a powerful blocking effect on
the AV node, thus slowing ventricular rate if the May respond to CSM No response to CSM
dysrhythmia is atrial in origin. It acts for only
Slowed with adenosine No response to
1520 seconds and is relatively safe in experienced
adenosine
hands. Its use should be avoided in the asthmatic
and in the presence of dipyridamole, which
greatly prolongs its action. VENTRICULAR ECTOPICS
Ventricular ectopics (VEs) may be unifocal (each
ectopic will have the same shape) or multifocal
(different shapes). The pulse will be irregular.

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 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

An ECG is the only certain way to distinguish PAROXYSMAL SUPRAVENTRICULAR

this from other causes of irregular pulse. Their TACHYCARDIA
danger lies in the fact that an ectopic arising on
the apex of a T wave may produce ventricular
fibrillation. Clearly, the more ectopics there are,
the greater is the probability of this happening.
Treatment should be considered if the ratio of VE
to normal QRS is greater than 1:6 or if multifocal.
Lignocaine would be the treatment of choice. Figure 6.9 Paroxysmal SVT.

CLINICAL ASSOCIATION any tachycardia originating in the AV node,

VEs can occur in healthy people without
evidence of any disease. The incidence is higher
in older individuals. VEs also occur after MI,
with electrolyte disturbance (e.g. hypokalaemia
and hypomagnesaemia), in valvular heart disease,
with cardiomyopathies, hypoxia and digitalis
toxicity.
COMMON TYPES OF
ATRIAL TACHYCARDIA
SINUS TACHYCARDIA
atria or SA node
P waves can be of abnormal shape and may
or may not be seen
QRS width usually normal (may be wide
if associated bundle branch block)
may be associated with ST depression,
suggesting ischaemia
regular 150250/min
abolished/slowed by carotid sinus massage
and adenosine
treatment: verapamil, digoxin, b-blockade
(avoid in heart failure or with verapamil).

P wave P wave
ATRIAL FIBRILLATION

150/minute 180/minute

Figure 6.8 Sinus tachycardia.

regular up to 160/min or so in young

lesser maximum rate in older patients
normal P wave and morphology
gradual onset
treat cause hypovolaemia, anaemia,
pulmonary embolism, sepsis, etc.
Figure 6.10 Atrial fibrillation.
irregularly irregular; variable ventricular rate,
often 100180
very common postoperatively in surgical patients
associated with hypovolaemia, hypoxia and
electrolyte disorders

75
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

also associated with cardiopulmonary disease ATRIAL FLUTTER

(e.g. ischaemic or rheumatic heart disease)
no P waves, normal QRS.
Flutter waves ORS complexes

TREATMENT
The management of AF depends on the cause
and effects. Many new cases occur after surgery,
caused by hypovolaemia, hypoxia or electrolyte Figure 6.11 Atrial flutter.
imbalance, particularly hypokalaemia and
hypomagnesaemia. These episodes can be rapidly regular flutter P waves 300/min
treated by correcting the causal factors alone. regular normal QRS, variable AV block
Identify and treat any underlying problems that usually associated with cardiac disease
would cause these predisposing factors to recur. may respond to carotid massage, adenosine
When new AF causes serious adverse signs may reveal flutter waves
(particularly hypotension, shock, chest pain, atrial flutter and fibrillation may be present
heart failure, decreased conscious level or marked in the same patient
tachycardia > 140), urgent treatment is needed treatment: cardioversion, digoxin, verapamil
either with DC cardioversion or intravenous (care with digoxin).
amiodarone. Seek expert help immediately.
New AF, which does not cause serious adverse
LEARNING POINT
signs and which does not respond to the correction
of the factors listed above, is usually treated with Remember, in all the above cases, investigate
digoxin or amiodarone. Again, if problems persist the underlying cause!
or recur, or you are unsure, get expert help.
Long-standing AF can worsen after surgery if
usual drugs have been omitted. This is unlikely to
convert back to sinus rhythm without digoxin or
amiodarone. Ultimately, anticoagulation may need
to be considered.
correct general causes as above, particularly
hypoxia, hypovolaemia or hypomagnesaemia
DC cardioversion consider if acutely
decompensated or following recent onset
(more responsive)
digoxin if reversal is not urgent
amiodarone.

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 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

I aVR V1 V4 I aVR V1 V4

II aVL V2 V5 II aVL V2 V5

III aVF V3 V6 III aVF V3 V6

Figure 6.12 Left ventricular hypertrophy. Figure 6.13 Right ventricular hypertrophy.

LEFT VENTRICULAR HYPERTROPHY CLINICAL ASSOCIATIONS

A hypertrophied left ventricle has a greater
influence on the electrical axis of the heart and
causes left axis deviation. This gives the picture
of tall R waves in I and aVL with S waves in III
and aVF. Most noticeably, the increase in the left
ventricular muscle mass also produces tall R
waves in leads over the left ventricle (V4 to V6),
and deep S waves in leads over the right ventricle
(V1 to V3).
Conditions causing an increase in afterload or
work on the left ventricle, for example, aortic
valve disease, systemic hypertension.
RIGHT VENTRICULAR HYPERTROPHY
When the electrical activity of the hypertrophied
right ventricle predominates over the left, there
is right axis deviation (leads I, II, III) with a tall
R wave in V1 with deep S wave in V6. A tall
pulmonary P wave suggests right atrial hypertrophy.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CLINICAL ASSOCIATIONS W-shaped QRS in some of the reciprocal leads,

Conditions causing increased right ventricular
afterload, for example, pulmonary hypertension,
cor pulmonale, pulmonary stenosis.
LEFT BUNDLE BRANCH BLOCK
Electrical activity in the left ventricle is
delayed because conduction to it must take place
via the right ventricle. The resultant delay in left
ventricular depolarisation produces the M-shaped
QRS wave, typically in V5, V6, I and aVL, and a
typically leads III and aVF.
RIGHT BUNDLE BRANCH BLOCK
Conversely, in right BBB, right ventricular
depolarisation occurs via the left ventricle.
In right BBB the M-shaped QRS would typically
be in leads V1, V2 and V3. Right BBB with left
axis deviation suggests bi-fascicular block.
This condition will often need pacing seek
help early!

I aVR V1 V4 I aVR V1 V4

II aVL V2 V5 II aVL V2 V5

III aVF V3 V6 III aVF V3 V6

Figure 6.14 Left bundle branch block. Figure 6.15 Right bundle branch block.

78
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

CLINICAL ASSOCIATIONS MYOCARDIAL INFARCTION

Coronary artery disease, valvular heart Ischaemic heart disease is very common,
disease, ventricular hypertrophy and fibrosis, particularly in the elderly or in patients with
cardiomyopathies. peripheral or cerebro-vascular disease or diabetes
mellitus. Peri-operative MI has a higher mortality
than that occurring remote from operation. A
BRADYARRYTHMIAS
recent MI (< 6 months) should preclude elective
Slow heart rates are problematic if associated surgery since the incidence of peri-operative MI
with hypoperfusion or hypotension (Table 6.8). is increased within this period. ALL cardiac drugs
They are common in the elderly. The patient should be continued up to and including the day
likely to get troublesome heart block (e.g. those of operation and recommenced at the earliest
with bi-fascicular block) should be detected opportunity postoperatively. Peri-operative MI is
pre-operatively and considered for elective pacing. often silent, though may present with shortness
In the patient with symptomatic bradycardia, of breath, hypotension, evidence of decreased
atropine (0.61.2 mg) may help but pacing may organ function (including confusion) secondary
be needed. Isoprenaline infusion may be used to cardiogenic shock, acute dysrhythmias, sudden
under guidance of an intensivist or cardiologist. pulmonary oedema or cardiac arrest. It should
Discuss with your medical or ICU colleagues also enter the differential diagnosis of acute
sooner rather than later! upper abdominal pain. A high index of suspicion
is required particularly in high-risk groups.
TABLE 6.8 The ECG may show typical changes of anterior,
anterolateral or inferior MI with ST-segment
CONDITIONS ASSOCIATED WITH elevation of > 1 mm in the relevant leads
BRADYCARDIA overlying the infarct (primary changes) and
Autonomic inversion in the leads opposite to it (reciprocal
Pain, especially visceral changes). T waves flatten and invert within hours
(may also be associated with tachycardia) to days of MI and Q waves develop over 12
Raised intracranial pressure days. Changes may be masked by a pre-existing
Drugs: -blockers left BBB and new BBB should make you suspicious.
The ECG may be normal after an MI, certainly
Nonautonomic
for the first hour or so. A normal ECG therefore
Myocardial infarction (particularly
does not exclude MI.
inferior MI)
Gram-negative sepsis
Hypoxia
Drugs digitalis toxicity
Hypothyroidism
Hypothermia.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

PRACTICE POINT TABLE 6.9

Recognition of patterns of ECG changes in MI:

TIME OF ECG CHANGES AFTER MI
Anterior infarct primary changes V1, V2,
V3, V4 Change Onset/duration
Inferior infarct primary changes II, III, aVF Peaked T waves Seconds
Posterior infarct isolated ST depression ST changes (usually elevation) Hours
V1, V2 Q waves Hoursdays
Treatment T wave inversion Hoursdays
Oxygen, analgesia refer and transfer to
high-care area
ANTERIOR MYOCARDIAL INFARCTION
Raised ST segments in V1V4.
Early treatment influences outcome significantly.
If you suspect the presence of an MI then seek the
advice of a physician urgently. In the meantime:
check and correct the ABCs
make the patient comfortable with a suitable
opiate analgesic. Morphine (or diamorphine)
is best, titrated to response intravenously
(12 mg boluses every 2 minutes). Cyclizine
(50 mg) or metoclopramide (10 mg) I aVR V1 V4
intravenously can be used to prevent or
treat nausea
give high flow oxygen to reduce hypoxia
(monitor SaO2)
give glyceryl trinitrate (sublingual or spray)
to reduce coronary artery spasm. Nitrates also
have a synergistic effect with thrombolysis
II aVL V2 V5
arrange appropriate investigations: (i) ECG
(serial ECGs are required); and (ii) blood tests
to exclude anaemia and electrolyte disturbances,
and for troponin levels.
ECG changes of MI are localised to ischaemic
or infarcted areas whereas generalised changes
are seen in, for example, hyperkalaemia (peaked
T waves) or pericarditis (ST elevation). The timing III aVF V3 V6
of changes is shown in Table 6.9.
Figure 6.16 Anterior MI.

80
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

INFERIOR MYOCARDIAL INFARCTION ACUTE TREATMENT OF PROVEN

Raised ST segments and Q waves can be seen
in II, III, aVF leads (with reciprocal ST depression
in leads I, aVL and V2V4). Non-pathological Q
waves can be present in leads II and III. Compare
this with the example of the anterior infarction
above.
MYOCARDIAL INFARCTION
THIS SHOULD BE INSTITUTED BY THE
CARDIOLOGY TEAM BUT WILL REQUIRE
CLOSE LIAISON WITH THE SURGICAL TEAM:
THERE WILL NEED TO BE DISCUSSION
REGARDING RISK OF BLEEDING VERSUS
BENEFIT OF INTERVENTION, ANTICOAGULATION
AND ANTI-PLATELET TREATMENT.

Acute treatment involves: (i) aspirin; (ii)

clopidogrel; (iii) primary percutaneous intervention
followed by anticoagulation with heparin or low
molecular weight heparin; (iv) glycaemic control,
I aVR V1 V4 particularly in diabetic patients (BM < 11 mmol/l);
and (v) -blockers (providing there is no evidence
of cardiac failure, bradycardia or hypotension,
-blockers have been shown to improve survival).
If primary percutaneous intervention is not
available, the fibrinolytics streptokinase or
Alteplase (rTPA) can be used, particularly if there
II aVL V2 V5 is persistent chest pain and gross ECG changes,
though not in the immediate (< 2 weeks) post-
operative period because of the risk of bleeding.
Other contra-indications to fibrinolytics include:
previous streptokinase treatment (further
streptokinase contra-indicated use rTPA)
active peptic ulcer
III aVF V3 V6
previous haemorrhagic stroke
recent head injury, however minor
Figure 6.17 Inferior MI. prolonged traumatic CPR.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
ACUTE CORONARY SYNDROMES
Acute coronary syndrome is an increasingly
used all-encompassing term that refers to a variety
of myocardial conditions and includes acute
MI (both Q wave and non-Q wave) and unstable
angina. The full range of conditions included is
listed in Table 6.10.
In most of these patients, the development of
an acute coronary syndrome is due to rupture or
erosion of an atherosclerotic plaque within the
walls of a coronary artery, leading to thrombus
formation. This is then followed by platelet
aggregation and vasoconstriction of the associated
vessels. Less commonly, an acute coronary
syndrome is the result of emboli or coronary spasm.
It is often impossible to distinguish between the
different causes clinically.
TABLE 6.10
THE ACUTE CORONARY SYNDROMES
Acute myocardial infarction
Transmural myocardial infarction
Q wave myocardial infarction
ST elevation myocardial infarction (STEMI)
Non-Q wave myocardial infarction
Sub-endocardial infarction
Non-ST elevation myocardial infarction
(non-STEMI)
Unstable angina
82
TREATMENT STRATEGIES
AGAIN, THIS WILL NEED TO BE INSTITUTED BY
THE CARDIOLOGY TEAM FOLLOWING SURGICAL
DISCUSSION REGARDING RISK OF BLEEDING
VERSUS BENEFIT OF ANTICOAGULATION AND
ANTI-PLATELET TREATMENT.
measure serial Troponin levels
aspirin
clopidogrel
anticoagulation
glycaemic control BM < 11 mmol/l
-blockade
It is likely that patients with acute coronary
syndromes will require further cardiology review
and investigation prior to discharge.
CONGESTIVE CARDIAC FAILURE
CCFis common in surgical critical care. It varies
in severity from mild dyspnoea, which is easily
treated, to cardiogenic shock. Demands on the
heart are increased by surgical illness and this
may unmask or worsen cardiac failure.
Cardiac function depends on preload, intrinsic
myocardial function and afterload. This concept
can be simplified in the following way. If the
heart is thought of as a simple pump, the preload
is analogous to the priming of the pump; it will
only work well if it has something (and not too
much) to pump. Ensuring adequate cardiac filling
is essential. Any condition which disturbs pump
filling will affect preload and therefore cardiac
function (Table 6.11a).
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

Intrinsic myocardial function is analogous to the

function of the pump itself; if the pump fails in TABLE 6.11
any way, it will not be able to cope with the
demands made on it. Any condition that directly CAUSES OF CARDIAC FAILURE IN
affects the function of cardiac muscle will affect SURGICAL CRITICAL CARE
intrinsic myocardial function (Table 6.11b). (a) Conditions affecting preload
Afterload can be thought of as the work that is hypovolaemia (bleeding, inadequate volume
demanded of the pump to overcome the resistance replacement, etc.)
to forward flow. If the resistance to flow is low, fluid overload
less work will be required of the pump; if it is pneumothorax/cardiac tamponade
high, the pump will have to work harder to produce (b, c as well)
an equal output. Conditions that alter circulatory
(b) Conditions affecting intrinsic myocardial
resistance (systemic or pulmonary vascular
function
resistance) or cause an obstruction to flow will
ischaemia
affect afterload (Table 6.11c). Increases in afterload
infarction
raise the cardiac oxygen demand, yet there is
dysrhythmias
decreased supply to the sub-endocardial areas as
chronic heart failure + operative stress
the contracting muscle squeezes the sub-endocardial
hypocalcaemia and other electrolyte
capillaries. If there is a simultaneous tachycardia
disturbances
the diastolic time interval is reduced and the
myocardial depressant factors (e.g. in sepsis )
coronary artery blood flow is reduced, decreasing
pneumothorax/cardiac tamponade
myocardial oxygen delivery even more.
(see a, c as well)
(c) Conditions affecting afterload
aortic/pulmonary valvular stenosis
pulmonary embolism
pneumothorax/cardiac tamponade
(see a, b as well)
aortic dissection

After surgery, a patient may develop CCF as a

result of any of the conditions listed in Table 6.11.
Sometimes, multiple factors apply in a single case
and the range of specific disease processes that may
produce these problems is wide. Most commonly,
it is as a result of fluid overload. The cause of
fluid overload may be obvious (e.g. giving blood
or parenteral nutrition simultaneously with

83
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
maintenance fluids to a patient with borderline
cardiac function). Fluid balance can also become
positive insidiously perhaps as a result of several
days of giving slightly too much maintenance
fluid to a small, elderly patient, who may also have
had routine diuretics omitted or developed AF.
The pathophysiolgy of CCF is such that patients
enter a downward spiral of increasingly inefficient
cardiac function. The physiological response to
the failing heart (as it is to surgical pathology)
is to increase catecholamine release in an attempt
to stimulate cardiac output. Unfortunately, the
failing heart has a flat Starling curve: one
shifted down and to the right compared to the
curve in Fig. 6.18. It is unable to respond and
maintain cardiac output by increasing its stroke
volume and tends to rely on an increase in rate.
This is inefficient in that diastole is short, which
reduces the time available for diastolic filling
(affecting preload) and for perfusion of the coronary
arteries leading to development of relative or
absolute ischaemia (and further affecting intrinsic
myocardial function).
Decreasing afterload
Increasing contractility
150
Stroke volume (ml)
100
50
0 anxiety and dyspnoea
0 10 20
Ventricular filling pressure (mmHg)
Figure 6.18 Cardiac function: Starling curve
Cardiogenic pulmonary oedema occurs with
acute LVF or during an exacerbation of CCF. The
patients usually have hypertension and ischaemic
heart disease and are often elderly. They may
develop symptoms as a result of MI or acute
ischaemia precipitated by pain from non-cardiac
sources. Sudden withdrawal of epidural analgesia
may cause acute afterload increases in susceptible
patients while increasing preload as the sympathetic
block wears off. The commonest causes are
iatrogenic fluid overload, dysrhythmia and MI.
Patients become acutely dyspnoeic, orthopnoeic
and tachypnoeic. They are tachycardic, sweaty,
often hypertensive and a gallop rhythm may be
present with a high JVP. They become hypoxic
with increased work of breathing, which further
aggravates myocardial ischaemia. Chest auscultation
reveals crepitations basally with some wheeze
(cardiac asthma) and, if very severe, pink, frothy
sputum may be produced. The CXR may show
fluid in the horizontal fissure, peribronchial
cuffing, upper lobe diversion, perihilar bats-wing
appearance and, rarely, Kerley B lines.
PRACTICE POINT
Treatment follows ABC principles:
oxygen, sit the patient up, CPAP/BIPAP
as soon as practicable
diuretics and small doses of opiate
intravenously to aid vasodilation
reduce afterload as well as decreasing
30
if intravenous vasodilators/inotropes
considered, transfer to high-care area.
84
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT

CASE SCENARIO 6.2

A 65-year-old woman with long-standing ischaemic heart disease had a right mastectomy 2 days
ago. You are asked to see her on the third postoperative day because she has become acutely short
of breath following an episode of severe central chest pain which lasted about 10 min but has
since settled. When you arrive on the ward, the patient is obviously dyspnoeic and is unable to
speak in complete sentences. She looks very unwell, and her skin feels cool and clammy. The staff
nurse who is with her reports that her pulse rate is 110 bpm and her blood pressure is 170/95. You
ask the nurse to give the patient high flow oxygen, using a mask with a reservoir bag. You examine
the patients chest and find that she has a respiratory rate of 28 breaths/min and fine crepitations
up to the mid zones on both sides. It is difficult to hear her heart easily but you do not think you
can hear any murmurs, although you think she has a gallop rhythm. Her blood pressure is now
140/90. You ask the nurse to help you sit the patient up and establish intravenous access. An
examination of the patients ward charts shows that she was progressing well until this episode.
The case notes revealed that she is hypertensive, has occasional angina (about one attack every
2 weeks associated with exercise or cold weather) and usually takes bendrofluazide 2.5 mg and
atenolol 50 mg each morning. From the prescription, it seems that she has not had these since
her operation as she has felt nauseated due to the morphine PCA she has been using until recently.
Although she seems slightly better with the oxygen and re-positioning, you decide to give her
a dose of frusemide 40 mg i.v. You ask for an ECG to be obtained and order a CXR. The ECG shows
a sinus tachycardia of 100 bpm but is otherwise unchanged from the one obtained pre-operatively.
The CXR confirms pulmonary oedema. You arrange for the patient to be transferred to the high
dependency ward where she can have continuous ECG, saturation and blood pressure monitoring
and ask for her to be reviewed by the cardiology team. In the meantime, you arrange for routine
blood tests and cardiac enzymes to be sent.

LEARNING POINTS
treat the ABCs first!
give high flow oxygen to all patients during initial assessment
many symptoms can be helped or relieved by repositioning of patients
transfer to a higher level of care when closer monitoring is required
seek expert help early.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

The acute management of heart failure is as follows: and reducing preload by diuresis may worsen
assess and treat ABCs cardiac output. If the afterload is high, reducing
give oxygen and monitor SaO2 it by using vasodilators may be beneficial but
stop i.v. infusions (may be only temporary subsequent worsening hypotension may be
measure) detrimental to myocardial perfusion. Accurate
drugs: consider diuretics (e.g. frusemide 80 mg individualised treatment requires the measurement
i.v.), nitrates (patch, sublingual, buccal or i.v.), of cardiac output, preload and afterload so
diamorphine 2.55 mg i.v. (but be sure of invasive cardiac monitoring is required to optimise
diagnosis opiates can kill a patient with acute fluid loading, inotropic support and/or vasodilator
asthma or chronic bronchitis) therapy. Senior critical care input and monitoring
12-lead ECG is urgently needed.
treat any underlying cause such as dysrhythmia,
pulmonary embolus or tamponade
RISKS OF SURGERY
CVP monitoring
early specialist referral. It is very important to be aware of the risks of
surgery in the patient with ischaemic heart disease
Cardiogenic shock occurs when there is severe
and, particularly, of the risk of re-infarction (Table
impairment of cardiac function with hypotension
6.12). It should be evident that delaying surgery,
of less than 90 mmHg or 30 mmHg less than the
if at all possible, will have a marked effect on the
patients normal systolic pressure is present.
outcome.
The patient may be tachycardic or bradycardic.
Amongst the causes, the commonest is severe
myocardial ischaemia or infarction. The cardiac TABLE 6.12
output falls, systemic hypotension occurs and
RISK OF CARDIAC DISEASE
there is progressive fall in organ perfusion.
IN NON-CARDIAC SURGERY
Left ventricular end diastolic pressure rises and
pulmonary venous pressure increases, which leads Higher Lower
to pulmonary oedema formation. The patient
becomes dyspnoeic and hypoxic and a downward Recent MI MI > 6 months
spiral develops as low SaO2 and low diastolic Unstable angina Stable angina
pressure further compromises myocardial perfusion.
The acutely failing heart is exquisitely sensitive to Severe aortic stenosis Abnormal ECG
too much or too little fluid. The patient normally Decompensated Compensated
has pulmonary oedema so increasing preload with heart failure heart failure
i.v. fluid is often detrimental. Occasionally, the
failing heart can have a high preload requirement Severe hypertension Compensated
valvular lesions

Cardiac arrhythmias Cardiomegaly

86
 CHAPTER 6 | CARDIOVASCULAR DISORDERS, DIAGNOSIS AND MANAGEMENT
The risk of peri-operative MI is greater with
abdominal and thoracic surgery and is related
to the duration of operation. The chance of
re-infarction has been estimated as:
60% if within 3 weeks of MI
27% if MI within 3 months of procedure
11% if MI within 36 months of procedure.
The presence of cardiac failure pre-operatively
indicates a significant anaesthetic risk.
Measurement of the ejection fraction can help
quantitate this.
HYPERTENSION
For a patient with chronic hypertension, avoid
stopping long-term anti-hypertensive medication
suddenly unless the patient is hypotensive.
Remember to review the prescription chart of
patients on cardiac drugs on a daily basis. As
with almost all cardiac medication, it should be
given on the morning of surgery and re-instituted
as quickly as possible afterwards. Many anti-
hypertensive drugs have side effects including
hypokalaemia (diuretics), hyperkalaemia (ACE
inhibitors) and impaired responses to hypovolaemia
(vasodilators and -blockers).
Acute, life-threatening hypertension is rare. If the
blood pressure is sustained at 220/120 or above
with signs of organ dysfunction, involve cardiology
immediately.
87
PACEMAKERS
Patients who have pacemakers not infrequently
require surgery. Pacemakers can vary between the
simple fixed rate type (although these are rarely
used now) to the complex demand type. They
can be bipolar or unipolar, the casing acting as
the return earth in the latter. It is vital to be aware
that your patient has a pacemaker because the use
of diathermy can inhibit the demand type, though
this is less likely to cause problems with a standard
fixed rate type. The important points are:
any patient who has a pacemaker and requires
surgery should have had a recent cardiology
review to ensure the pacemaker is functioning
optimally
the diathermy earthing pad should be placed
as far away from the pacemaker as possible
(e.g. on the thigh or under the buttocks). Never
place the pad on the back of the patient behind
the pacemaker
use short bursts of diathermy rather than long ones
bipolar diathermy is safer than unipolar
avoid using diathermy near the pacemaker
if possible
always monitor the ECG during any procedure.
Pacemaker types are classified using a 3 or 4 letter
code. Classification is based on which chambers
are paced, the response of the pacemaker to a
sensed beat and programmability. Recognition of
the codes and details of pacemaker function are
beyond the scope of this manual and the CCrISP
course. If you have any doubts or worries contact
a cardiologist!
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

SUMMARY
the detection and treatment of early clinical
signs can prevent major deterioration
abnormal signs must be acted on quickly
patients deteriorate rapidly from cardiovascular
problems
normal clinical findings do not always exclude
significant abnormality further investigations
and monitoring can help
new and long-standing cardiac disorders occur
frequently in surgical patients be aware of
common management strategies
impaired perfusion, hypotension, end-organ
dysfunction and poor response to treatment
suggest severe problems
patients with acute abnormalities of
cardiovascular function should not be left
without a clear management plan including
appropriate treatment and a timely re-assessment
higher levels of care are often required either
pre-emptively if the patient has long-standing
problems pre-operatively, or in response to
acute events
seek specialist help (anaesthetic/cardiology/ICU)
as appropriate at an early stage.

88
7
Shock and
haemorrhage

89
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
define shock
understand the various aetiologies of shock
recognise the clinical features of a patient
with shock
initiate early treatment of the shocked
patient
based on the history, clinical condition
and response to treatment, decide on an
appropriate level of care.
This chapter aims to give a practical clinical
overview rather than a detailed account of the
pathophysiology of shock.
DEFINITION
Shock may be defined as acute circulatory
failure, with inadequate tissue perfusion
causing cellular hypoxia.
Regardless of the underlying cause, shock is
characterised by an acute alteration of the
circulation in which inadequate perfusion leads
to cellular damage, dysfunction and failure of
major organ systems.
The clinical features of shock are so variable that
they cannot be used to define the shocked state.
Although the terms hypotension and shock are
often taken to be synonymous, cellular perfusion
may be inadequate despite a normal blood pressure.
Perfusion describes blood flow but also implies
the supply of substrates (including oxygen) and
the removal of waste products. Use of the
90
terminology inadequate tissue perfusion rather
than reduced perfusion is important since blood
flow and substrate supply may be increased in
hypercatabolic states (e.g. trauma and sepsis)
and yet inadequate for the demands of the tissues
due to increased metabolism and failure to
extract substrates from the circulation, especially
in septic shock.
In the shocked state, the distribution of blood flow
is important. While certain viscera preserve flow
through autoregulation (e.g. heart, kidney), others
cannot (e.g. skin, gut) and may be hypoperfused
preferentially. Intestinal hypoperfusion may occur
in the face of a normal pulse and blood pressure
and, following a brief hypotensive episode, a
prolonged period of intestinal hypoxia may occur,
with generation of cytokines and the onset of
systemic inflammation.
LEARNING POINT
Patients may be in shock despite a normal
systolic blood pressure.
AETIOLOGY OF SHOCK
All patients with shock can be regarded as
having generalised failure of the circulation.
There are four principal categories of shock:
(i) hypovolaemic;
(ii) vasodilatory or apparent hypovolaemia;
(iii) cardiogenic; and
(iv) obstructive (see Fig. 7.1 and Table 7.1).
Within this classification, the various different
causes of shock have common mechanisms with
regard to the clinical manifestation of shock
and these can be considered in terms of preload.
 CHAPTER 7 | SHOCK AND HAEMORRHAGE

Preload Heart Afterload

Cardiogenic Vasodilatory
Hypovolaemia MI, CCF, Arrythmia Sepsis
Haemorrhage
Obstructive Neurogenic
Fluid loss
Anaphylactic
Dehydration PE, tamponade
Adrenal Insufficiency
pneumothorax

Figure 7.1 Classification of shock in relation to the effect on the circulation.

Rapid assessment of the patient may quickly

TABLE 7.1
suggest the cause of shock. Keeping this in mind,
classification helps to avoid the risk of a given
COMMON MECHANISMS OF SHOCK
diagnosis being overlooked. Of course, the patient
may have more than one factor contributing to Hypovolaemia Blood or fluid loss
the shock state: for example, a patient with
Cardiogenic Pump failure
abdominal sepsis where the primary problem is
vasodilation but where hypovolaemia due to ileus Septic Early vasodilation
also contributes. Late pump failure
Fluid loss from
capillary leak
Neurogenic Vasodilation
Anaphylactic Vasodilation and
pump failure
Obstructive Prevents venous
return to the heart

91
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
HYPOVOLAEMIC SHOCK
Stroke volume dictates cardiac output, and is
directly linked to ventricular filling pressure by
the Starling curve (Fig. 7.2). Remember that the
curve can be shifted up and to the left by inotropes
and sympathetic stimulation. It is important to
consider the Starling curve when thinking about
the clinical manifestation of shock, but also
rationale and response to treatment. Hypovolaemia
is the commonest cause of shock in the surgical
patient. The low cardiac output is a direct reflection
of reduced venous return (preload). It may result
from any of the following causes:
haemorrhage is a common cause of
hypovolaemia. Its effects vary with the duration
and severity of blood loss, the patients age
and myocardial condition, and the speed and
adequacy of resuscitation. It can be usefully
classified, in terms of assessment and guiding
treatment, by the degree of blood loss into
four stages: stage 1, < 500 ml; stage 2,
5001000 ml; stage 3, 10002000 ml; and
stage 4, > 2000 ml
loss of gastrointestinal fluid may result from
vomiting and diarrhoea, from fistulae, and
from sequestration of fluid in the bowel lumen
in intestinal obstruction
trauma and infection increase capillary
permeability with local sequestration of fluid and
oedema. In addition to causing hypovolaemia,
trauma and infection may lead to sepsis
burns lead to direct loss of fluid from the
burned surface and tissue fluid sequestration
renal loss of water and electrolytes (e.g. in
sodium-losing chronic nephritis, diabetic
ketosis or Addisonian crisis) is an occasional
cause of shock
frequently, iatrogenic surgical factors contribute
to hypovolaemia (e.g. poor fluid prescription,
92
slow or tissued intravenous infusion,
inappropriate use of diuretics, mechanical
bowel preparation, fasting prior to anaesthesia,
and insensible fluid losses during prolonged
operations and on going fluid loss from
dissected areas for some hours after surgery).
Decreasing afterload
Increasing contractility
150
Stroke volume (ml)
100
50
0
0 10 20 30
Ventricular filling pressure (mmHg)
Figure 7.2 Starling curve plotting ventricular filling pressure
(venous return) against stroke volume (cardiac output). The
curve is shifted up and to the left by sympathetic stimulation
or inotropic agents.
CARDIOGENIC SHOCK
Primary impairment of cardiac function may
result from myocardial infarction or ischaemia,
acute arrhythmias, acute cardiomyopathy, acute
valvular lesions (caused by aortic dissection or
trauma), and myocardial contusion.
OBSTRUCTIVE SHOCK
Secondary impairment to cardiac function can
result from obstruction to cardiac output. Causes
include cardiac tamponade producing constriction
of the heart, pressure on the heart from a tension
pneumothorax or major pulmonary embolism
with obstruction to right ventricular outflow.
In all shock states, myocardial performance is
affected adversely by reduced coronary arterial
 CHAPTER 7 | SHOCK AND HAEMORRHAGE

perfusion and, in some cases, by circulating
myocardial depressant substances (particularly
in septic shock).
NEUROGENIC FACTORS
True neurogenic shock follows spinal transection
or brain-stem injury with loss of sympathetic
outflow beneath the level of injury and consequent
vasodilation. The rapid increase in size of the
vascular bed, including venous capacitance vessels,
leads to reduced venous return and reduced cardiac
output. There is often a relative bradycardia. An
analogous condition may be seen during epidural
analgesia, although in this case, the block is seldom
high enough to cause a bradycardia.
ANAPHYLAXIS
Anaphylactic reactions are mediated by IgE
antibodies causing massive degranulation of mast
cells in sensitised individuals. Activation of mast
cells releases histamine and serotonin and, with
systemic kinin activation, this leads to rapid
vasodilation, a fall in systemic vascular resistance
(SVR), hypotension, severe bronchospasm with
hypoxia and hypercarbia. In contrast to sepsis,
the fall in SVR is so sudden and profound that
blood pressure falls markedly. Prompt treatment
with oxygen, fluids, adrenaline, hydrocortisone
and an antihistamine is required plus avoidance
of the trigger substance.
ENDOCRINE FACTORS
Although adrenal failure is in itself a potent
cause of shock due to the sudden withdrawal of
circulating cortisol and aldosterone, the role of
the adrenal cortex in the production of shock by
other causes is debatable. Acute adrenal failure
may occur in severe meningococcal sepsis
(WaterhouseFriedrichsen syndrome). Adrenal
insufficiency (often subacute) is also seen in
patients in whom necessary peri-operative steroid
cover has been omitted.
SEPTIC SHOCK
Sepsis and septic shock are complex and are
covered in more detail elsewhere. In septic shock,
the patient becomes hypotensive and the tissues
are inadequately perfused as a result of organisms,
toxins or inflammatory mediators. Common
sources include the abdomen, chest, soft tissues,
wounds, urine and intravascular lines (central or
peripheral) or other medical implants.

CASE SCENARIO 7.1

You receive a trauma team call to the emergency department the paramedics have radioed that
they will be arriving in 4 min with a 34-year-old patient who has a BP of 80 systolic and a stab
wound to the back between the shoulder blades.
WHAT FORM OF SHOCK MIGHT THIS PATIENT BE SUFFERING FROM?
Haemorrhagic shock? Pump failure due to pericardial tamponade? Pump failure due to tension
pneumothorax? Neurogenic shock due to spinal cord transection? All are possible!
WHAT ACTION MAY BE NECESSARY?
This depends on the cause, but immediate attention to the ABCs with administration of oxygen and
fluids, diagnosis and definitive treatment are the mainstays of treatment.

93
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
CLINICAL FEATURES OF SHOCK
ASSESSMENT
It is essential that you follow the systematic
approach of the CCrISP algorithm when assessing
the potentially shocked patient. Perform the
immediate assessment with simultaneous
resuscitation, followed by a full patient assessment,
including chart review, history, examination and
investigations. For a patient on a surgical ward,
it is also important to speak to the medical and
nursing staff, and note the results of recent
investigations and procedures.
IMPORTANT FEATURES TO NOTE
is there an obvious cause which requires
immediate treatment?
does the age or previous history of a
patient suggest a possible myocardial
component?
has the patient recently received medication
which may have an effect on the
cardiovascular or respiratory systems?
does the fluid balance chart of the patient
show a gradually deteriorating urine output
or likelihood of a significantly abnormal
fluid balance? Remember that trends in the
charted observations may be more important
than absolute values and that patients with
hypovolaemic shock may have a normal
systolic blood pressure
does the patient have a temperature, high
white cell count or a history of an
operative procedure which may make sepsis
a more likely diagnosis?
94
The majority of patients with shock have a low
cardiac output; an exception is septic shock where
the cardiac output may be increased. The classical
appearance of a patient with low-output shock
is that seen after haemorrhage. The features are
partly due to loss of circulating volume and tissue
perfusion, and partly to intense sympathetic
stimulation. Early diagnosis of shock depends
on recognition of the signs of decreased tissue
perfusion, particularly of the skin, kidneys and brain.
Signs of decreased tissue perfusion are summarised
in Table 7.2. These are accompanied by varying
degrees of tachycardia, hypotension and tachypnoea
proportional to the severity of the shock.
Increased respiratory rate is frequently seen
before significant tachycardia, but marked
tachypnoea is an important sign of impending
deterioration. Confusion and coma are late signs
of marked cerebral hypoperfusion, and blood
pressure is often maintained until severe shock.
TABLE 7.2
SIGNS OF DECREASED TISSUE PERFUSION
Cool peripheries
Poor filling of peripheral veins
Increased respiratory rate
Increased coreperipheral temperature
gradient
Capillary refill time prolonged (> 2 s)
Poor signal on pulse oximeter
Poor urine output (< 0.5 ml/kg body
weight/h)
Restlessness or decreased conscious level
Metabolic acidosis or elevated lactate levels

In haemorrhagic shock, decreased venous return
to the heart results in a low right atrial pressure,
low right ventricular end diastolic volume and
reduced right heart output. This usually reduces
the left atrial and ventricular end diastolic
volumes and stroke volume falls. Since cardiac
output (CO) = heart rate (HR) x stroke volume
(SV), for a fixed SV, an increase in HR is the
first compensatory measure available. The only
way the body has to increase the SV acutely is
to decrease the amount of blood contained in the
resistance and capacitance vessels by
vasoconstriction, squeezing the periphery to return
more blood to the heart. This gives the appearance
of the cold shut down peripheries. The patients
response to hypovolaemia may be modified in the
elderly, in ischaemic heart disease, in patients on
-blockers, trained athletes and young adults.
The effect of haemorrhage on blood pressure is
particularly variable. It depends on the duration
and magnitude of blood loss, the patients age and
cardiovascular status, and the speed and adequacy
of resuscitation. Initially, the systemic blood
pressure is maintained, and may actually increase,
particularly in young patients. The pulse pressure
may drop (difference between systolic and diastolic
pressure) as a result of peripheral vasoconstriction
but this is a subtle sign. Up to 25% (or even 30%)
of circulating volume can be lost without affecting
systolic pressure because of the intense
vasoconstriction and, to a lesser extent, the shift
of fluid from interstitial to intravascular space.
A modest further loss (to 3540% deficit) can
precipitate calamitous collapse, perhaps with
bradycardia rather than the expected tachycardia.
95
CHAPTER 7 | SHOCK AND HAEMORRHAGE
PRACTICE POINT
Systolic blood pressure may be normal in
the presence of significant loss of circulating
volume.
SPECIFIC FEATURES OF CARDIOGENIC SHOCK
Cardiogenic shock is inadequate tissue perfusion
resulting directly from myocardial dysfunction.
Common causes in surgical patients include
myocardial infarction, acute arrhythmias, post-
cardiac surgery myocardial stunning and cardiac
contusions from trauma. The clinical features are
similar to hypovolaemic shock. Although there
is no primary loss of circulating volume, cardiac
output falls and catecholamine-induced
vasoconstriction produces cool clammy peripheries,
reduced capillary return, reduced urine output
and reduced level of consciousness. The picture
is modified, however, by elevation of cardiac
filling pressure leading to elevation of the central
or jugular venous pressure and pulmonary oedema,
but low arterial pressure.
A careful history and examination of the chest,
heart sounds (there may be a gallop rhythm or
associated murmur), neck veins together with
assessment of a chest radiograph and ECG should
prevent the possibility of cardiogenic shock being
overlooked in a surgical patient. Echocardiography
may be valuable.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

SPECIFIC FEATURES OF OBSTRUCTIVE SHOCK

TABLE 7.3
Cardiac tamponade, tension pneumothorax and
pulmonary embolism are the principal causes of
CLINICAL FEATURES OF SEPSIS
obstructive shock. Through a variety of mechanisms,
each restricts the work of the heart, leading to a Early Late
drop in the CI. Typically, the JVP can be elevated
Restlessness and Decreased conscious
in each and assessment of the JVP should be
slight confusion level
routine. Tamponade and tension pneumothorax
need prompt intervention to relieve the pressure Tachypnoea Tachypnoea
on the heart, but all can respond temporarily to
Tachycardia Tachycardia
intravenous fluids and oxygen.
Low SVR
SPECIFIC FEATURES OF SEPTIC SHOCK
High cardiac output Low cardiac output
Sepsis is dealt with and defined elsewhere in this
book and further comments here are limited to Systolic BP normal Systolic BP less than
the making of a diagnosis. Clearly, haemodynamic or slightly decreased 80 mmHg
instability and pyrexia 57 days after a colonic
Oliguria Oliguria
resection with anastomosis should be treated with
suspicion but, in general, the early features of Metabolic acidosis, Metabolic acidosis,
sepsis (Table 7.3) are subtle, diagnosis is difficult elevated blood lactate elevated blood lactate
and a high index of suspicion is essential. The
Warm, dry, suffused Cold extremities
patient may look remarkably well, largely due
extremities
to pink, well-perfused extremities. As already
stressed, clues may be obtained from the history
or the patients charts; in postoperative patients, In septic shock, an early effect of the mediators
blood gas measurements can aid early diagnosis. is to cause a fall in SVR due to vasodilation. The
decrease in SVR reduces the afterload on the heart
PRACTICE POINT and leads to a reflex increase in cardiac output,
provided the patient has a healthy myocardium
A grave error is for inexperienced personnel
and adequate volume state. Thus, in early sepsis,
to treat restlessness (due to hypoxia and
blood pressure may be well maintained, and often
hypovolaemia) with sedation rather than
the patient is pink with flushed peripheries and
appropriate resuscitation.
maybe a low diastolic pressure. This is in contrast
to cardiogenic or pure hypovolaemic shock where
the SVR rises in response to the drop in cardiac
output.

96

In the later stages, or if the patient is already
hypovolaemic, the heart may be unable to maintain
an adequate output in the face of a falling SVR, so
that blood pressure falls (BP = CO x SVR). The
patient may then become almost indistinguishable
from someone suffering from hypovolaemic
shock. Hence, the patient may be hypothermic
or hyperthermic depending on the phase. As the
septic process progresses, fluid loss due to increased
capillary permeability may also contribute to
hypotension and, in addition, myocardial depressant
factors reduce cardiac function directly. Initially,
the patient requires oxygen and fluids but it is
vital that cultures are taken and the source is
identified and treated.
PRINCIPLES OF MONITORING
AND MANAGEMENT
Restoration of adequate perfusion at the cellular
level is the essential aim of treatment. In practice,
the initial resuscitation of patients with any form
of shock is influenced more by the nature of the
associated physiological disturbances than by the
specific underlying cause. On the other hand, the
ultimate success of treatment depends largely on
detection and elimination of the underlying cause
(e.g. arrest of bleeding or drainage of a source
of sepsis).
PRACTICE POINT
In monitoring and management, the essential
principles are:
resuscitate
diagnose
treat underlying cause.
97
CHAPTER 7 | SHOCK AND HAEMORRHAGE
The mainstays of early treatment are infusion of
fluid and oxygen administration with the aim of
improving cardiac output and oxygen transport.
If cardiogenic and obstructive forms of shock can
be excluded, all patients with shock can be initially
treated with fluid administration (initial bolus
10 ml/kg body weight crystalloid if normotensive,
20 ml/kg body weight if hypotensive). Oxygen
should initially be given in high concentration
(1215 l/min) until blood gas analysis or saturation
measurements are available.
Occasionally, you will encounter a patient with
major haemorrhage who requires operative
resuscitation. You will find it very difficult to
resuscitate a patient with major haemorrhage;
prolonged attempts are futile and merely lead
to coagulopathy, hypothermia and death.
Exsanguinating patients need immediate definitive
treatment usually by surgery.
As stressed above, it is the indices of tissue
perfusion which are most useful in the early
management of hypovolaemia. One should not
be misled into thinking that a patient is well
perfused simply because the blood pressure and
heart rate are normal. On the other hand, a lucid
patient with rapid capillary refill, warm dry skin,
and a good urine output is unlikely to have
significant hypovolaemia.
MONITORING AND INSTRUMENTATION
Successful clinical monitoring depends on the
frequent measurement of simple haemodynamic
indices and assessment of tissue perfusion, as just
outlined. The following guidelines apply to all
forms of shock.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Venous access
Good venous access must be obtained early by
inserting at least two large-bore (16G) peripheral
cannulae. Access is normally obtained in the
antecubital fossa or via the cephalic vein at the
wrist. If vasoconstriction makes it difficult to
gain access, a cut-down can be performed in the
antecubital fossa or on the long saphenous vein
in front of the medial malleolus. In profoundly
shocked patients, it may be necessary to obtain
the initial access by cannulating the femoral vein
percutaneously in the groin. Draw blood for urgent
cross-matching, haematology and biochemistry.
Bladder catheterisation
A bladder catheter is inserted transurethrally
unless there is a possibility of urethral injury
(as in severe pelvic fractures), or when dealing
with young children. Under these circumstances,
a suprapubic catheter is inserted once the bladder
has filled, under ultrasound control. The urinary
catheter is attached to a graduated collecting
device (urimeter) so that output can be measured
hourly.
Electrocardiogram (ECG) monitoring
ECG monitoring will detect arrhythmias and
myocardial ischaemia. It is indicated particularly
in primary cardiogenic shock, myocardial
dysfunction secondary to ischaemia, direct thoracic
injury, and sepsis. Arrhythmias are more likely
when there is electrolyte or acidbase disturbance.
Pulse oximetry
A pulse oximeter attached to a finger or ear
lobe allows transcutaneous estimation of oxygen
saturation of haemoglobin. The accuracy of such
peripheral probes depends on good peripheral
perfusion. However, in poorly perfused patients,
98
good equipment gives a visual or audible warning
of a poor signal, so providing a useful index of
both oxygen transport and tissue perfusion.
Central venous catheterisation
A catheter can be inserted percutaneously via the
internal jugular or subclavian veins so that it lies in
the superior vena cava, thus allowing measurement
of CVP. In the initial resuscitation of an overtly
hypovolaemic patient, time must not be wasted
inserting a central venous catheter. The small bore
and length of the catheter usually prevent rapid
infusion, while inadvertent damage to the apical
pleura during insertion may lead to a pneumothorax,
a potentially fatal complication in a patient who
is not resuscitated. Furthermore, central lines are
no longer the remit of the junior surgeon and
should be placed by anaesthetists in a controlled
environment with the use of ultrasound guidance.
However, following the initial administration of
fluid and oxygen, measurement of CVP can be
useful, particularly in severe shock and if there is
clinical uncertainty.
In a shocked patient, a low (< 5 mmHg) or even
negative CVP indicates the need for more fluid. At
the other extreme, a very high CVP (> 20 mmHg)
may indicate cardiac failure and the need for
diuretics, vasodilators or inotropic agents, or an
obstructive cause. In practice, static measurement
of CVP can mislead. For example, a young patient
may have an apparently normal CVP (say 10
mmHg) as a result of vasoconstriction. A fluid
challenge can resolve doubt. This is performed by
measuring CVP before and after the administration
of a small fluid bolus (100200 ml). If the CVP
does not rise, further fluid can be given safely; a
significant rise in CVP suggests myocardial failure
or dysfunction and avoids inadvertent
overtransfusion (Fig. 7.3).
 CHAPTER 7 | SHOCK AND HAEMORRHAGE

or patients who are bleeding. Subsequent

16 administration depends on monitoring the response
14 to treatment and all shocked patients need careful
12 and repeated assessments (Table 7.4).
10
CVP cmH20

8
TABLE 7.4
6

4 CONTINUING ASSESSMENT OF THE

2 SHOCKED PATIENT
0
0 1 2 time (ml) 4 5 6 Monitor clinical appearance, noting
200ml fluid bolus restlessness and confusion (cerebral hypoxia),
well-filled
redistributing respiratory rate and state of the peripheral
hypovolaemic
circulation

Figure 7.3 CVP response to a 200-ml bolus in different clinical Monitor pulse rate, systemic blood pressure,
situations. hourly urine output and CVP
Gain valuable additional information by
monitoring or periodically checking:
CORE AND PERIPHERAL blood urea and electrolyte concentrations
TEMPERATURE MEASUREMENT haemoglobin concentration, white cell
Using ones own hand to assess skin temperature count and haematocrit
is useful in shocked patients. If thermistors are used ABGs
to measure core and peripheral temperatures, the blood lactate level
coreperipheral gradient provides a useful index pulse oximetry
of skin perfusion. Core temperature measurement core and peripheral temperature
also detects hypothermia, as in trauma patients CI
who have been exposed to a cold environment,
Remember to send appropriate samples for
particularly following water immersion.
bacteriological examination (e.g. blood, urine,
sputum, drain fluids) when sepsis is suspected,
FLUID ADMINISTRATION
and cardiac monitoring/serial ECGs in
In most cases, the type of fluid lost in shock has
cardiogenic shock
little influence on the choice of fluid for initial
replacement. Successful initial resuscitation Most importantly, diagnose and treat the
depends more on the rapidity and adequacy of underlying cause
fluid replacement than on the choice of regimen.
Initial fluid management consists of boluses of
warmed crystalloid (1020 ml/kg body weight).
However, red cell concentrates may be required
at an early stage, particularly amongst the injured

99
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Infusion of large volumes of fluid (of any type,
including red cell concentrates) can cause dilution
of clotting factors (factors II, V, VII, IX, X and
platelets). The resulting coagulopathy may need
correction by transfusion of fresh frozen plasma,
platelets and cryoprecipitate. This should be done
selectively rather than routinely but a watch must
be kept for evidence of coagulopathy. Hospitals
usually have guidelines for the use of clotting
factors and you should be aware of these.
Considerable degrees of coagulopathy can be
simply observed and monitored in the absence of
active bleeding, but clotting factors are required
early if the patient is bleeding or surgery is
likely. Hypothermia also contributes to a bleeding
diathesis by causing platelet dysfunction. Ensure
that resuscitation fluids are warmed, particularly
when massive transfusion is needed.
Colloid or crystalloid?
Synthetic colloids increase circulating volume
to a greater degree in the short term per volume
infused, but most are redistributed within a few
hours in a similar manner to saline. All carry
a risk of side effects, notably anaphylaxis and
coagulopathy. You should recall to which fluid
compartment each fluid type is distributed and
also the mechanisms whereby circulating volume
is supported by the extracellular and intracellular
compartments during hypovolaemic states.
The debate over colloid or crystalloid is well
documented. Some of the salient points are:
in most situations, both types of fluid are able
to replenish blood volume if given in sufficient
quantity
to replace a given amount of blood loss, the
volume of crystalloid is approximately three
times that of colloid
100
when crystalloid resuscitation is used, there
is a greater weight gain and probably more
oedema than when colloid is used
there is no fixed relationship between serum
albumin concentration and colloid osmotic
pressure until serum albumin falls below 15 g/l
in septic shock with increased capillary
permeability, both colloids and crystalloids
pass across the vascular basement membrane
colloid can interfere with coagulation under
some circumstances
many experienced practitioners would limit
the volume of colloid used during resuscitation
to < 50% of non-blood fluid or 11.5 l,
whichever is less.
More importantly, the principal changes in
practice that occur with experience are the
early identification and rapid treatment of
hypovolaemic states, a prompt utilisation of
blood when haemorrhage is occurring and,
most importantly, the surgical treatment of any
underlying cause, particularly haemorrhage.
ASSESSMENT OF RESPONSE
One of the most important steps in the management
of the shocked patient is the assessment of the
response to treatment. For every exsanguination,
you will meet many more patients who become
critically ill with shock in a less dramatic, but
no less important manner. During resuscitation
and no more than every 30 minutes or so, you
should re-assess the patients progress. If the signs
are not improving, you need to change your plan
of action (Table 7.5). The aim is to detect those
patients you have initially misjudged or those
who are temporary responders. These patients are
common and it can be difficult to assess the need
for surgery. Involve senior help if you are in doubt.
 CHAPTER 7 | SHOCK AND HAEMORRHAGE

CASE SCENARIO 7.2

You are called to see a 68-year-old man on the surgical ward. He is 5 days postoperative following
a difficult anterior resection for a colonic tumour. He weighs 125 kg, has NIDDM, and a history of
hypertension. He has been spiking a temperature for the last 48 h but has remained reasonably
well until now. It is 8 p.m., and the nurses on the ward are concerned because he has become cold,
clammy and restless. You follow the CCrISP protocol and establish that the airway is clear. His SaO2
is 92%, respiratory rate 28 per min, pulse 110 and the urine output has been 20 ml over the last
hour. He is restless but co-operative.
WHAT FORM OF SHOCK MIGHT THIS MAN HAVE AND WHAT WOULD YOU DO?
Hypovolaemic/haemorrhagic shock? Cardiogenic shock? Septic shock? Obstructive shock? All are
possible and there may be more than one pathology here. He has been spiking a temperature, so
sepsis is possible. This might also have led to a secondary haemorrhage. He has risk factors for
cardiac disease, and myocardial infarction or acute arrhythmia, possibly related to sepsis, is quite
possible. He may also have had a pulmonary embolism causing obstructive shock. Following the
CCrISP protocol, you should quickly be able to ascertain which type of shock is most likely. You
institute high flow oxygen, gain intravenous access and send blood samples including cross-match
and cultures. The BP is 115/60 which you note from chart review has dropped. His urine output has
also tailed off. Abdominal examination is difficult but feels tense. There is no acute change on ECG.
HOW WOULD YOU FURTHER MANAGE THIS SITUATION?
This man is clearly shocked and needs simultaneous assessment and resuscitation. The response to a
fluid challenge while you wait for available results will give you a much better idea of the problem.
You give a fluid challenge of 20 ml/kg body weight and re-assess. His BP initially rises to 140/80,
but then drops again and he remains restless and tachycardic. On a blood gas, his Hb is 7 g/dl, and
he has a metabolic acidosis with lactate of 5.
WHAT ACTION MAY BE NECESSARY?
The most likely cause here is secondary haemorrhage, possibly secondary to intra-abdominal sepsis.
He is a temporary responder and needs further intervention (probably surgery) to deal with the
cause. You must seek help at this stage! As a bare minimum, he needs a higher level of care, with
invasive monitoring and further aggressive resuscitation.

LEARNING POINTS
There may be more than one cause of shock the CCrISP system will help you to decide.
Shock may not be amenable to resuscitation alone surgery may be required to stop the
bleeding or deal with the cause.
Some surgical patients are difficult to assess if you are not sure, or a patient fails to
respond to simple resuscitative measures, get help early.

101
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Algorithm of cardiovascular monitoring/support

TABLE 7.5
RESPONSES TO TREATMENT OF SHOCK
No response, e.g. exsanguination
Temporary response, e.g. continuing slow
but steady postoperative haemorrhage
Full response, e.g. simple sepsis caused
by repeat urinary catheterisation which
responds to resuscitation and antibiotics
REFRACTORY SHOCK
If hypovolaemic shock proves refractory to fluid
replacement and oxygen administration, the
factors shown in Table 7.6 may be responsible.
TABLE 7.6
An algorithm of cardiovascular monitoring/support
is given in Table 7.7. Many surgical patients
become hypovolaemic and present with oliguria,
hypotension, tachycardia, hypoxia or acidosis in
isolation or almost any combination. Many do not
develop a full picture of shock but require prompt
treatment just the same. Most are simply treated
with conventional measures including adequate
fluid replacement (and other necessary treatments).
You need to have a method of management clear
in your mind. You should review them later to
ensure that normal function has definitely been
re-established. Patients who need anything more
than simple correction of minor-to-modest fluid
deficit should be managed in a high-dependency
environment.

REFRACTORY SHOCK
Underestimation of the degree of
hypovolaemia
Failure to arrest haemorrhage
Presence of cardiac tamponade or tension
pneumothorax
Underlying sepsis
Secondary cardiovascular effects due
to delay in instituting treatment
Further action is necessary!

102

TABLE 7.7
ALGORITHM OF CARDIOVASCULAR
MONITORING/SUPPORT
1. Establish and maintain normovolaemia
Assess with CCrISP system
Give reasonable intravenous fluid challenge
(1020 ml/kg crystalloid initially, see text)
Treat any underlying cause (blood loss,
sepsis, etc.)
Determine recent fluid balance
2. Assess response
Clinically (perfusion, BP, urine output,
JVP, pulse)
By simple investigations (repeat FBC, pulse
oximetry, pH, BE)
Improving, adjust fluid regimen, treat
underlying cause, plan to review shortly
Deteriorating, resuscitate and involve expert
help directly
No progress, re-assess different diagnosis,
treat and seek help; still hypovolaemic,
continue fluids and find/treat cause
Not sure if normovolaemic, insert CVP and
seek higher level of care
3. CVP
Inadequate, establish normovolaemia
Adequate c > 8 cmH2O), but inadequate
circulation: re-assess cause (and treat as
necessary); consider inotrope in higher level
of care; no/poor response, seek help directly
High c > 15 cmH2O), and patient exhibits
signs of cardiac failure: simple LVF, treat;
suspect cardiogenic shock, call for help
4. Invasive monitoring and inotrope treatment
Transfer to ICU
CHAPTER 7 | SHOCK AND HAEMORRHAGE
Remember to treat any underlying pathology,
particularly haemorrhage (which often needs
surgery), in addition to giving intravenous fluids
and oxygen.
Patients who have incipient failure of more than
one system need the help of an intensivist directly
and, in any event, you should have a very low
threshold for involving help and informing your
consultant. All these patients should be receiving
monitored oxygen therapy.
Young and fit patients tolerate rapid infusion
well and CVP insertion is indicated when there
is doubt about progress, adequacy of filling or
likely tolerance of the administered fluid.
Patients who continue with inadequate
cardiovascular function and in whom good
cardiovascular filling has been confirmed by
CVP measurement may require inotropic support.
In these cases senior help should be mandatory
and patients should be treated in a critical care
environment. In some units, local protocols may
allow administration of a single inotrope outside
the intensive care unit, but these should be
administered cautiously with a low threshold
for transfer to the (ICU), with whom the case
should already have been discussed.
Metabolic monitoring in refractory shock
Urea and electrolyte levels are required to establish
a baseline and monitor progress. Arterial pH and
blood gas measurements are essential to assess
hypoxia, hypercapnia and acidbase balance.
Blood lactate levels are a good index of cellular
hypoxia and hepatic function.
103
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Metabolic acidosis associated with inadequate
perfusion will correct rapidly once cardiac output
is improved; indeed, its disappearance is a marker
of adequate resuscitation. It is rarely necessary
to give bicarbonate.
Respiratory acidosis with an increase in arterial
PaCO2 usually indicates the need for endotracheal
intubation and assisted ventilation.
Higher levels of care
Shock is an immediate life-threatening condition
and demands treatment as such. The ability of the
cardiovascular system to compensate has been
discussed and shock reflects the state which is
reached once decompensation is occurring. While
uncomplicated hypovolaemia can often be managed
satisfactorily without intensive care facilities,
patients with severe trauma, sepsis, cardiogenic
shock or shock complicated by secondary
myocardial dysfunction will all benefit from the
monitoring and support available in an ICU.
Consideration should be given to early ICU
admission for patients with significant co-morbidity,
since ICU can then play a prophylactic role.
Similarly, patients who fail to respond quickly
and completely should be discussed with ICU and
a surgical consultant. Assessment and monitoring
of the cardiovascular system is detailed elsewhere.
The basis of ICU care is the same as outlined
previously with attention to fluid administration,
oxygenation and definitive treatment.
104
Based on the underlying cause of shock and
measurement of cardiovascular parameters
(particularly the confirmation of an adequate
circulatory volume), some patients require inotropic
support. The selection of an inotropic agent is
based on the cardiovascular effects of the drug
and the underlying pathophysiology. The
cardiovascular effects of many agents can be
predicted from a knowledge of their particular
effect on adrenergic receptors (see Chapter 8).
SUMMARY
Definition
acute circulatory failure, with inadequate
tissue perfusion causing
cellular hypoxia.
Diagnosis
assess perfusion and not simply blood pressure
identify the different common patterns.
Treatment
restore perfusion
common initial approach with oxygen and
fluids except for cardiogenic
treat underlying cause
determine appropriate level of care.
8
Cardiovascular
monitoring
and support

105
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the indications for cardiovascular
monitoring and support
be familiar with the methods used
understand how drug and fluid therapy
may be used to manipulate cardiovascular
function.
INTRODUCTION
Maintaining adequate tissue perfusion and hence
oxygen delivery is one of the primary goals in the
management of the critically ill surgical patient.
The main predeterminant of oxygen delivery
is cardiac output; therefore, monitoring and
therapeutic manipulation of cardiac output are
essential components of critical care practice.
Cardiac output is, in turn, determined by preload,
cardiac function and compliance, and afterload
(Fig. 8.1), all of which can be altered and monitored.
Preload Heart Afterload
Figure 8.1 The determinants of cardiac output.
106
In most patients, clinical assessment, vital signs,
urine output and simple tests such as core/
peripheral temperature gradients can provide
a suitable evaluation of cardiovascular function.
These will provide information on how well the
cardiovascular system is fulfilling its basic
function. The efficacy of the system in delivering
oxygen and nutrients to the tissues, and removing
carbon dioxide and other products of tissue
metabolism, depends upon the production of a
cardiac output sufficient to meet the demands of
tissue metabolism. Clearly, this is highly variable
depending on how well (or ill) a patient is.
Furthermore, the cardiac output must be regionally
matched to the metabolic needs of individual
organs.
In critically ill patients, deviation from the
normal ranges of any of these components of
cardiac output can occur unexpectedly, rapidly
and with little to see clinically in the early stages
of deterioration. Clinical assessment alone may
well be inadequate and the accuracy of estimation
of volume status compared to more intensive
monitoring techniques may be as low as 30%.
Objective measurements showing change should
be detected as early as possible to allow rapid
corrective therapy before vital organ damage
has occurred. Modern monitoring equipment
can provide rapid, accurate and reproducible
measurements of cardiovascular performance
and the effects of treatment.
Cardiovascular therapy in the critically ill aims
to avoid tissue hypoxia and the degree to which
one must go to monitor the adequacy of the
cardiovascular system in achieving this goal
varies with severity of illness and complexity of
the case. Organs vary in their ability to maintain
their own perfusion (through autoregulation);

generally, measurements relate the total body
picture, rather than adequacy of perfusion of
specific viscera. Certain organs, notably the gut,
are prone to hypoxia and this hypoxia may
continue to drive the inflammatory process
(including multiple organ failure) even once the
initial causal factors have been dealt with. To
overcome this, one approach has been to try and
ensure that the critically ill patient with multiple
organ failure has a circulation that provides an
oxygen delivery which is, if anything, greater
than normal, thus minimising the chance of
occult hypoxia. A related approach has been
to monitor plasma lactate level and/or negative
BE on the grounds that elevated values of these
suggest that tissue hypoxia may be present.
An alternative strategy is to try and measure
specific visceral perfusion (such as that of the
intestine) by techniques such as tonometry.
There is much to be said for pursuing similar
objectives, at an appropriate level, in all unwell
patients and particularly in the pre-operative
preparation of the critically ill surgical patient.
In broad terms, the indications for intensive
monitoring of the cardiovascular system are:
failure to restore promptly and maintain
cardiovascular homeostasis with simple
techniques (i.v. fluids, surgery, non-invasive
blood pressure, pulse oximetry)
during procedures which may give rise to rapid
or profound changes in preload or afterload
during treatment with vaso-active drugs
which influence preload, afterload or myocardial
function, to monitor response to treatment
and guide management strategies
in any patient who has, or is at risk of
developing, a low perfusion state from any
cause.
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CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT
The parameters that can be monitored include:
blood pressure
CVP
cardiac output or CI.
MEASUREMENT OF BLOOD PRESSURE
Non-invasive intermittent measurements of
arterial blood pressure can be performed using
an automated sphygmomanometer. However,
non-invasive readings can be erroneous if size
or positioning of the cuff is incorrect. Automated
devices are useful to demonstrate trends in blood
pressure and are reliable in most stable patients.
In more unstable patients, more accurate readings
are required using invasive techniques, whereby
mechanical energy of blood pressure changes are
converted to electrical energy using a transducer,
allowing continuous monitoring on a screen.
CVP monitoring utilises the same principles and
shares the same potential pitfalls as arterial
pressure monitoring.
TRANSDUCERS
While the physical principles of how these
individual measurements are made are beyond
the scope of this course, certain basic scientific
principles apply. Changes in any parameter to
be measured must be detected accurately with
sufficient sensitivity, over the range required,
at a suitable frequency response often from
inaccessible sites and converted by a transducer
so that the signals vary in proportion to the changes
in the parameters under study. A transducer
converts the mechanical energy of pressure
changes to electrical energy in a manner such
that the electrical output of the transducer varies
directly with the change in pressure. An example
of this kind of system is shown in Fig. 8.2.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Pressure bag
Monitor
Flush device
Transducer
Arterial cannula
Figure 8.2 Signal transduction from an arterial cannula.
The pressure wave is transmitted from the artery
(in this case) to the transducer through relatively
rigid tubing. The transducer converts the
mechanical signal to an electronic one, displayed
on the monitor. The three-way tap on the
transducer allows zeroing. Patency of the
cannula is maintained by a slow constant flush
of heparinised saline under pressure and most
systems incorporate a button for bolus flushing
to clear any debris and improve the signal.
The electrical signals must be displayed and
processed so that derived results may be calculated.
The measurement system must be zeroed and
calibrated. If pressure is measured, this should
be done with the transducer level relative to the
108
point within the patient at which the pressure is
to be measured. Care should be taken to minimise
the interference and damping of the measurement
signal to ensure optimal signal to noise ratio.
Failure to zero or calibrate will produce erroneous
results. This can also happen when the cannula
or catheter is kinked, abuts the vessel wall or is
partly occluded by clot.
SAFEGUARDS
Before considering the individual techniques, one
should be aware of certain ground rules common
to all procedures used during invasive monitoring
methods:
a sound knowledge of relevant practical
anatomy
competency in the technique of insertion of
the line
the procedure should be explained to the
patient
all procedures must be performed using
aseptic technique
contra-indications and complications must
be known
the benefit accrued must exceed the risks of
the procedure
the patient must be in the care of people who
know how to manage the lines, all of which
must be Luer-locked to prevent disconnection
all lines should be clearly labelled and
injections into or sampling from lines ONLY
performed at designated sites
attendants should be familiar with the
monitors to ensure that the data derived from
them are accurate
lines must be dressed aseptically and changed
at appropriate intervals.
 CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT

ARTERIAL PRESSURE MONITORING

A peripheral artery can be cannulated either to Pressure on
allow continuous measurement of arterial blood arteries and
elevation to
pressure by connecting the cannula to a transducer,
blanch hand
or to allow for repeated sampling of arterial blood
for analysis. The radial artery is the most frequent
anatomical site, followed by the dorsalis pedis
artery, and a 20G or 22G sized cannula is used.
The brachial and femoral arteries should be avoided
if possible because of lack of collaterals and, in
the case of the femoral site, the risk of sepsis.
Th
When using the radial artery, always check for
ulnar flow supply to the palmar arch using Allens
test prior to cannulation (Fig. 8.3). Local sepsis Little finger
a)
and coagulopathy are the main contra-indications
while complications include haematoma,
thrombosis, distal ischaemia, intimal damage, false
aneurysm formation, disconnection and injection Release
of irritant drugs. Samples from arterial cannulae pressure
should be taken aseptically and the line flushed
and re-sealed afterwards. After cannulation of
the artery, the cannula should be connected to
a continuous-flush device containing heparinised
saline under pressure which maintains patency
and allows blood pressure changes to be conducted
without letting blood flow out of the artery into
the line.

b)

Figure 8.3 Allens test. Blanch the hand by clenching the

fist then simultaneously occlude radial and ulnar arteries at
the wrist. An adequate pink flush of the hand on release of
the ulnar pressure confirms an adequate ulnar supply to
the palmar arterial arches.

109
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

TECHNIQUE FOR RADIAL ARTERIAL

PUNCTURE/CANNULATION
Flexor carpi
Abductor radialis tendon Position and palpate
pollicis longus position the hand and yourself comfortably,
Radial artery
tendon
with adequate light and assistance
Radial palpate the artery with 2 fingers
styloid
feel and imagine its course above and below
the point of entry
insert at 45, avoiding the superficial vein
which often overlies.
Puncture
advance needle tip in a linear fashion
do NOT wiggle it around!
if you miss, re-palpate and search in
a systematic fashion with further straight
Puncture Advance guidewire insertions
let syringe fill and withdraw
pressure haemostasis 5 min.
Cannulation: the Seldinger technique
puncture as above
advance guide wire
railroad cannula
check backflow and secure cannula
Railroad cannulation Connect and secure connect transducer and flushing set-up.

Figure 8.4 Technique for radial arterial puncture/cannulation.

110

If the arterial cannula is to be used for pressure
monitoring, it is connected via a relatively short
length of rigid tubing to a 3 way tap, flush device
and transducer. Check that the transducer is
zeroed, calibrated at the correct level and that the
lines contain no air bubbles, which would cause
damping of the signal. The arterial waveform gives
real-time information about the blood pressure and
heart rate, but also modern computer algorithms
can transform pressure changes into shifts in
stroke volume or cardiac output. Often these need
to be calibrated by an independent mechanism
in order to compensate for the different levels of
vascular compliance seen between and within
patients. The morphology of the individual
waveform can also give information with regards
to the systemic vascular resistance and cardiac
contractility in both normal and pathological
conditions. In particular, a sharp peaked up-swing
and down-swing with a low dicrotic notch can
reflect significant hypovolaemia, but it is dangerous
to draw such conclusions unless the system is
adequately damped (Fig. 8.5).
mmHg
(a)
100
100
0 0
Figure 8.5 Arterial waveforms showing influence of damping:
a) adequately damped; b) underdamped; c) overdamped.
CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT
The changes in the arterial pressure trace with
the fluctuations in intrathoracic pressure during
artificial mechanical ventilation can be used to
determine patients who will respond to a fluid
challenge by increasing their stroke volume.
These changes can be characterised either by
the systolic pressure variation, the pulse pressure
variation or, nowadays when combined with a
cardiac output monitor, the stroke volume variation.
CENTRAL VENOUS
PRESSURE MEASUREMENT
CVP measurement is one of the most commonly
used monitoring tools in critical care, indicating
preload of pulmonary circulation and a rough
guide to systemic preload given a number of
provisos. The CVP is simply the pressure within
the SVC as it enters the right atrium, and reflects
the ability of the right heart to accept and deliver
circulating volume. The CVP is influenced by
various factors, including venous return, right
heart compliance, intrathoracic pressure and
(b) (c)
100
0
111
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
CENTRAL VEIN CANNULATION
Infraclavicular subclavian route
tilt the patient 20 head down, arms by the side
and head turned away from the side of entry
make a skin nick and insert the cannula 12 cm
below the mid point of the clavicle
advance horizontally towards the suprasternal
notch remember, advance needle tip in a
linearfashion do NOT wiggle it around
try and visualise the anatomy beneath as
you do it think where your needle tip is,
particularly in relation to clavicle and pleura,
and the narrow gap between clavicle and first
rib, where the subclavian artery and vein run
if you miss, search in a systematic fashion
with further straight insertions, trying to
picture where the vein is most likely to be
when venous blood is aspirated freely, remove
syringe and insert the guide wire
Figure 8.6a Infraclavicular subclavian vein cannulation using
the Seldinger technique.
112
leave enough guide wire outside to let you
railroad the catheter over it without losing
the wire inside the patient
advance the catheter to a previously measured
point, so the tip lies in the distal SVC
secure the catheter and check its position by
chest X-ray.
Ultrasound image of the jugular vein and
carotid artery
using ultrasound, the vein is located at the
medial border of sternomastoid, at the level
of the thyroid cartilage and anterolateral to
the carotid artery
displace the artery medially and, under ultrasound
guidance, advance the needle through a skin nick
advance inferiorly at 30 to the skin, parallel
to the artery but lateral: this is often towards
the ipsilateral nipple
puncture and proceed as above.
Figure 8.6b Ultrasound image of the jugular vein and
carotid artery

patient position. While absolute measurements
of CVP are useful (with the normal range 08
mmHg or 010 cmH2O), often the trend in CVP,
and response to fluid challenge or therapeutic
manoeuvre is more important. This is particularly
useful when trying to deduce the cause of shock
(see Chapter 7).
CVP ACCESS
The route for access to the central venous
circulation depends on the skill and experience
of the operator and the presence of site-specific
contra-indications such as local sepsis,
coagulopathy, abnormal anatomy, operative site
and previous vein usage. While the techniques
are illustrated in Figure 8.6a, it should be noted
that the UK National Institute for Health and
Clinical Excellence (NICE) recommends that
ultrasound imaging should be used to guide
placement of central venous catheters into the
internal jugular vein in elective situations. NICE
further recommends that all those involved in
placing central venous catheters should undertake
training to achieve competence in the use of
ultrasound for this purpose. Ideally, ultrasound
should also be used in emergency cases, though
the anatomical landmark method is still
recommended for the subclavian route.
The internal jugular site is advantageous in
terms of a lower rate of complications, but is
uncomfortable and difficult to dress. The subclavian
route entails a higher risk, in particular the risk
of pneumothorax and intrathoracic bleeding,
which can be difficult to control.
113
CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT
PRACTICE POINT
No-one inexperienced in the technique
of central venous catheterisation should
undertake the procedure.
CVP MEASUREMENT
The best zero reference point, which represents
the level of the SVC, is the mid-axillary line at the
4th intercostal space, with the patient supine. The
alternative, the 2nd intercostal space at the sternal
edge, represents a point about 5 cm above the
atrium. For readings to be comparable at separate
times, they should always be taken from the same
point. The pressure may be measured using either
a liquid manometer filled with sterile dextrose
5% or by an electronic transducer reading over
a suitable pressure range in centimetres of water
(Fig. 8.7).
The water manometer is cheap, effective and
simple and can be used on ordinary wards but
does not respond to rapid changes in pressure.
Its response time is, however, sufficiently fast
to show the fluctuation in CVP with inspiration
(fall in pressure) and expiration (rise in pressure),
a change which confirms that the manometer
is reflecting the normal change in CVP with
fluctuation of intra-thoracic pressure. The
electronic transducer is faster and the analysis
of the signal produced allows the mean pressure
to be displayed taking into account the variation
with the respiratory cycle. The set up of the
transducer is identical to that for arterial
pressure measurement.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Giving set

Manometer
Position of the three-way
top for recording

Zero to sternal edge

b
b=a5
5
a

To central line

Figure 8.7 Liquid manometer for CVP.

CVP WAVEFORM INDICATIONS FOR CVP MEASUREMENT

The CVP waveform has a characteristic pattern fluid replacement therapy for hypovolaemia
that reflects changes in atrial pressure during the when conventional access is not possible, when
cardiac cycle as shown in Fig. 8.8. concern exists about over-transfusion or when
there is uncertainty about fluid volume status.
Central vein cannulation is NOT advocated as
A a primary route of access because of the risk
C
of complications and low flow rates achievable
(remember Poiseilles law)
V
to measure the effect of vaso-active drugs
X
Y
on venous capacitance, particularly vasodilators
to aid diagnosis of right ventricular failure,
when a high pressure will be seen in the
presence of poor cardiac output.
Figure 8.8 The CVP waveform. A wave, atrial contraction;
C wave, bulging of the tricuspid valve into the right atrium;
X descent, atrial relaxation; V wave; rise in atrial pressure prior
to tricuspid valve opening; and Y descent, atrial emptying.

114

PRACTICE POINT
CVP does not equal intravascular volume
and is not an indicator of left ventricular
function.
PITFALLS IN PRACTICE
inaccurate readings as a result of failure
of zeroing or calibration, placement of the
cannula tip in the right ventricle, tricuspid
regurgitation and incompetence, AV
dissociation and nodal rhythms
variations in intravascular volume,
sympathetic tone, cardiac output, intrathoracic
pressure (particularly during positive pressure
ventilation) may lead to a false impression of
a much higher right ventricular filling pressure
than is actually present (Fig. 8.9)
before using the line and acting on measurements
made, always check for easy aspiration of
blood, pressure fluctuation with respiration
and confirmation of position on X-ray
complications of central line insertion are
numerous and relate to damage to the veins
themselves and adjacent structures.
Complications include rupture of vessel and
haemorrhage with local haematoma or
haemothorax, tension pneumothorax
(particularly if the patient is on positive
pressure ventilation), air embolism, extravascular
catheter placement, knotting of catheters,
catheter breakage, catheter misplacement,
neurapraxia, arterial puncture, lymphatic
puncture, tracheobronchial puncture and sepsis.
Do not underestimate the potential severity of
central line sepsis.
115
CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT
General
anaesthetic
a b c d e
Figure 8.9 CVP and intravascular volume: pitfalls in the
shocked surgical patient: a, normal; b, shocked but compensating
(by peripheral vasoconstriction) with low CVP; c, rapid re-fill
and (temporarily) high CVP; d, redistribution and falling CVP as
degree of compensatory vasoconstriction lessens; and e, general
anaesthesia with vasodilatation, loss of compensation and very
low CVP.
All staff involved in the care of patients with
central venous access should be familiar with the
saving lives high impact care bundle for central
venous catheters. The Health Act 2006 Code of
Practice states that NHS organisations must audit
key policies and procedures for infection prevention.
The high-impact intervention approach to central
venous catheters provides a focus on elements
of the care process to prevent catheter-associated
infections. These comprise aspects regarding
line insertion, including aseptic techniques,
skin preparation and hand hygiene, and on going
care of the line, including regular inspection,
aseptic techniques and regular replacement of
administration sets.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
MEASUREMENTS OF CARDIAC
OUTPUT/CARDIAC INDEX
In shock states, the delivery of oxygen to the
tissues is at least as important as the level of
systemic arterial pressure. Global oxygen delivery
is a product of cardiac output and arterial oxygen
content. Cardiac output is, therefore, a pivotal
variable in the management of the critically ill
surgical patient.
The understanding of the relationship between
cardiac output and other parameters allows an
estimate of systemic vascular resistance, using
the following equation:
Cardiac output = Driving pressure
(MAPCVP)/systemic vascular resistance
Therefore, with a measurement of cardiac
output, MAP and CVP, an estimate of SVR can
be calculated and the combination of variables
used to guide rational decisions about volume
resuscitation and vasoactive therapies.
The pulmonary artery catheter (PAC or
SwanGanz catheter) has long been the gold
standard for advanced haemodynamic monitoring.
Pulmonary artery pressure and pulmonary artery
occlusion (or wedge) pressure can be used to
monitor right heart function and preload of the
systemic circulation. This is largely achieved
using thermodilution techniques and a thermistor
on the PAC. However, it is highly invasive with
significant risks of serious complications and less
invasive cardiac output monitors are becoming
more available, translating into a declining use
on the critical care unit. Cardiac indexing corrects
any variable for patient size (Table 8.1).
TABLE 8.1
VARIABLES DERIVED FROM CARDIAC
OUTPUT MEASUREMENTS
Systemic vascular resistance (SVR)
If too high (vasoconstriction), tissue
hypoperfusion is likely
If too low, maintenance of an adequate
mean blood pressure will be difficult
Stroke volume (SV), stroke index (SI)
A major determinant of cardiac output
and governable by preload
Left ventricular stroke work index (LVSWI)
An index of the function of the systemic
side of the heart
Oxygen delivery (DO2)
An index of the oxygen delivered to all
tissues
Oxygen uptake (VO2)
Index of oxygen consumption
NON-INVASIVE MEASUREMENT
OF CARDIAC FUNCTION
There are several less invasive techniques,
including trans-oesophageal Doppler (TOD),
echocardiography, pulse contour cardiac output
with indicator dilution (PiCCO) and lithium
indicator dilution calibration system (LiDCO).
Trans-oesophageal Doppler
TOD uses the Doppler shift principle to make
measurements of blood velocity in the descending
aorta. A disposable Doppler probe contained at
the tip of a 90 cm x 5.5 mm probe is passed
down the oesophagus to lie at the level of the
116

descending aorta (around 3545 cm) and rotated
until the arterial waveform is displayed. This
appears as a triangular shaped waveform since
the shift signal is displayed as a velocity/time plot.
The shape of the waveform provides information
on preload, stoke volume and afterload (Fig 8.10).
The area under the curve represents the stroke
volume flowing through the descending aorta and
applying a factor determined from the patients
age, height and weight allows the stroke volume
to be calculated. A number termed the corrected
flow time (FTc) is calculated: it is low in hypo-
volaemia and may be used to derive SVR. The
disadvantage of the TOD is that the patient must
be anaesthetised and intubated to tolerate the
probe. It cannot be used in patients who have
coarctation of the aorta or who are on intra-aortic
balloon pumps.
a
c cold saline into a central vein is proportional to
b d
Time
Figure 8.10 Stylised TOD waveforms for vascular abnormality:
a, best waveform, normal configuration; b, failing left ventricle
decreased waveform height and low peak velocity. Giving inotropes
increases waveform height and restores velocity; c, hypovolaemia
narrow waveform base with decreased FTc (giving volume lengthens
flow time and widens waveform base); and d, high systemic
vascular resistance/afterload reduced waveform height and
narrow base.
117
CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT
Trans-thoracic and trans-oesophageal
echocardiography
Bedside echocardiography is becoming increasingly
available as the hardware becomes more portable
and more affordable. The main role in critical
care is the assessment of preload and cardiac
contractility before and after intervention, and the
diagnosis of major cardiac structural abnormalities
(pericardial tamponade, severe valvular and
regional wall motion abnormalities).
Indicator dilution and pulse contour analysis
Instead of measuring temperature changes in
the pulmonary artery, which requires a PAC,
a thermistor can be placed in the systemic arterial
circulation. PiCCO calculates cardiac output from
a peripheral arterial cannula providing beat-to-
beat information to a computer, which in turn
follows the heart rate and pressure waveform and
integrates the area under the curve. The accuracy
of the method is improved as the cannula contains
a sensitive thermistor allowing thermodilution.
The small drop in the temperature of arterial
blood that follows the injection of a bolus of ice-
cardiac output. The thermodilution measurement
is used to calibrate the continuous cardiac output
monitoring software which calculates changes in
cardiac output by analysing the pulse contour of
the arterial waveform. PiCCO requires recalibration
at regular intervals and becomes unreliable when
the arterial waveform is suboptimal, for example
with a kinked line, air or blood clots in the system
or any other cause of a damped trace.
Other indicators can be used to replace
thermodilution techniques. Lithium chloride,
for example, is injected into a central vein and
the lithium concentrations are subsequently
analysed with an ion-sensitive electrode (LiDCO).
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Here, the blood can be sampled from a normal CARDIOVASCULAR SUPPORT

peripheral arterial line. Several drugs interfere
with the lithium analysis and lithium is contra-
indicated in some patients. As in thermodilution,
lithium-dilution is combined with continuous
pulse contour analysis and similar recalibration
requirements and issues with damped arterial
traces apply.
USING VASO-ACTIVE DRUGS
In the normal heart, cardiac output is determined
by preload, afterload, heart rate, rhythm,
contractility and balance of oxygen demand
and supply. If the heart is damaged, for a given
preload or afterload, cardiac output will decrease.
This can be represented graphically either by
pressurevolume loops or by the more familiar
Frank Starling curve (see Chapter 7, Fig. 7.2).

TABLE 8.2

ACTION OF INOTROPIC AGENTS

Receptor Effect Clinical use

Noradrenaline -adrenoceptor agonist Arteriolar Septic shock with
vasoconstriction low SVR
Adrenaline - and -adrenoreceptor Positive inotropic Wide-spread in conditions
agonist, predominantly and chronotropic. of low cardiac output
1-adrenoreceptor at Vascoconstricts at
low dose high doses
Dopamine - and -adrenoreceptors. Low dose: splanchnic Used as first choice
Dopamine (DA) 1 and 2 vasodilation, increased inotrope in some HDUs
receptors renal and hepatic blood
flow (DA1). High dose:
vasoconstriction
Dopexamine DA1, DA2 and Increases splanchnic Controversial in
-adrenoreceptor agonist blood flow peri-operative optimisation
Dobutamine Similar to dopamine Reduces SVR and Cardiogenic shock
increases cardiac output

118

Invasive cardiovascular monitoring collects the
data which allows the construction of such curves
so that the effects of varying preload, afterload,
inotropes, etc. can be accurately recorded,
ensuring that therapy is producing an objective
improvement in the patients cardiovascular
status. The curves are time consuming to plot and
often variations in fluid loading, vasodilatation
and inotropic support are taken on the basis of
repeated or continuous CI measurements.
If the CI remains low after correcting any
hypovolaemia with a fluid challenge, inotropic
or other vaso-active drugs are used with the aim
of optimising myocardial contractility by balancing
myocardial oxygen supply and demand. Accurate
measurements of derived variables can predict
probable therapeutic regimens.
Drugs that increase cardiac output and ejection
fraction are known as inotropes. Ideally, in
addition to these properties, they should reduce
afterload and preload, resulting in decreased
trans-ventricular wall tension, promoting coronary
blood flow, increasing myocardial oxygen delivery
and reducing oxygen consumption. Regrettably,
the ideal inotrope does not exist but the most
commonly used are adrenaline, noradrenaline and
dobutamine. They all act by providing an upward
left shift in the Starling curve as shown in Figure
7.2. Noradrenaline has a specific use in septic
shock as a vasopressor: it is used to increase
and maintain SVR within the normal range.
119
CHAPTER 8 | CARDIOVASCULAR MONITORING AND SUPPORT
Vasodilators such as sodium nitroprusside or
nitrates are of use when pulmonary oedema
occurs in heart failure, although they can produce
a reflex tachycardia if the blood pressure falls.
Occasionally, both inotropes and vasodilators
are used in combination (e.g. adrenaline and
nitroglycerine in severe LVF).
Inotropes and vasodilators can only be used safely
where a full range of monitoring is available.
They should never be used on ordinary surgical
wards and NEVER in the presence of hypovolaemia.
Their dose ranges, modes of delivery, etc. are
outside the scope of this course; your task is to
recognise the clinical conditions that mandate
their use and refer the patient to the appropriate
level of care.
SUMMARY
adequate cardiovascular function is a
pre-requisite for survival
to determine cardiovascular function accurately
and to control manipulative therapy, invasive
monitoring is necessary
all techniques have complications
the monitoring utilised should be appropriate
to the specific case in question.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

120
9
Renal failure,
prevention and
management

121
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the functions of the kidney
anticipate and predict patients at risk of
developing acute renal failure
outline the initial management of a patient
with acute renal failure and associated
life-threatening emergencies
know the common causes of acute kidney
injury in the critically ill surgical patient and
the five rules of renal failure
be aware of the implications of chronic
kidney disease in the surgical patient.
Abnormal renal function is common in surgical
patients and poor urine output is one of the most
common reasons for a trainee being called to
see a patient. The kidneys have a wide range of
functions and play a vital role in homeostasis.
In the context of the critically ill patient, they can
also be seen as bilateral retroperitoneal indicators
of cardiovascular stability.
Acute renal failure (ARF) in critically ill patients
is associated with a mortality of around 20% and
is often preventable, particularly with attention
to careful fluid balance. It is the responsibility
of the surgical team to anticipate and prevent
ARF where possible. When it occurs, treatment
122
is essentially supportive but the team must be
vigilant for the life-threatening complications
(hyperkalaemia, pulmonary oedema) and know how
and when to refer for renal replacement therapy.
FUNCTIONS OF THE KIDNEY
The primary functions of the kidney are:
elimination of water-soluble waste products
of metabolism other than carbon dioxide
elimination of water-soluble drugs
fluid and electrolyte homeostasis
acidbase balance
blood pressure control: reninangiotensin
system
endocrine function: erythropoietin and
vitamin D production
PHYSIOLOGY OF RENAL FUNCTION
The kidney regulates fluid and electrolytes by
filtration, secretion and re-absorption. Renal
blood flow is around 20% of cardiac output (1000
ml/min in an adult) and renal plasma flow (RPF) is
approximately 600 ml/min. The glomerulus filters
125 ml/min of renal plasma. This glomerular
filtration rate (GFR) is a much more reliable marker
of renal function than plasma creatinine. Most of
this fluid is re-absorbed, with only 1% passed as
urine (0.51 ml/kg/h). The kidney autoregulates
its plasma flow over a wide range of mean arterial
pressure (MAP). However at low MAP, RPF and
GFR become supply dependent and urine output
decreases this is the kidney protecting itself
from further reduction in perfusion pressure (Fig.
9.1). This is reversible in the short term but the
kidney is much more vulnerable to other insults,
particularly the tubular cells deep in the medulla,
which is more poorly perfused than the cortex.
 CHAPTER 9 | RENAL FAILURE, PREVENTION AND MANAGEMENT

140

120

100
Autoregulation

GFR (ml/min
80

60

40

20

0
0 20 40 60 80 100 120 140 160 180 200 220 0 100 200 300 400 500 600 700 800 900 1000
Main Arterial Pressure Serum creatinine (mol/L)

Renal Plasma Flow (RPF)

Glomerular Filtration Rate (GFR) 20 year old 90kg male
Urinary Output 80 year old 50kg female

Figure 9.1 Autoregulation maintains a steady glomerular Figure 9.2 The glomerular filtration rate steadily decreases with
filtration rate through a wide range of renal perfusion pressures. age, but this is not evident in raised creatinine until a relatively
low level is reached.

The plasma creatinine level and GFR are inversely RENAL FAILURE
related. If the plasma creatinine level drifts outside There are 5 golden rules of renal failure in the
the normal range, the GFR may already be 50% surgical patient:
of normal. It is important to recognise that a
borderline creatinine may pose an increased risk
of ARF, particularly in the elderly as the GFR 1. The kidneys cannot function without
decreases with age (Fig. 9.2). adequate perfusion.
2. Renal perfusion is dependent on adequate
blood pressure.
PRACTICE POINT
3. A surgical patient with poor urine output
normal adult urine output is 1 ml/kg/h usually requires more fluid.
oliguria is < 400 ml/day (< 17 ml/h)
4. Absolute anuria is usually due to urinary
anuria is < 100 ml/day.
tract obstruction.
5. Poor urine output in a surgical patient is
not a frusemide deficiency.

123
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 9.1

8 hours following an elective abdominal aortic aneurysm repair, a 68-year-old man develops oliguria
despite receiving 100 ml of 0.9% saline per hour and with no major change in pulse rate or blood
pressure. There have been no obvious signs of haemorrhage or excess loss from the nasogastric tube.
The CVP is 10 cmH2O but the HDU nurse feels the trace is unreliable and positional, and suggests
the patient is sub-optimally perfused. Haemoglobin is 11.1 g/dl. The junior trainee recommends a
dose of frusemide (80 mg i.v.) to improve the urine output. This improves the urine output to 100
ml for 2 h, after which it falls again to 20 ml/h. The on-call senior trainee prescribes a further
dose of frusemide (40 mg i.v.) by telephone. This has no effect and the ICU consultant is contacted.
He re-sites the CVP line and the measurement is found to be very low. Immediate circulatory volume
expansion, however, does not restore urinary output. By the next day, the plasma creatinine and urea
levels have risen rapidly and renal replacement therapy is required. The patient has a long and
complicated course and dies of multiple organ failure 3 weeks later.

LEARNING POINTS
adequate renal perfusion is the critical factor this is often simply achieved with careful
attention to fluid balance
insensible and tissue fluid losses continue after surgery postoperative hypovolaemia is
common and may not be caused by acute postoperative haemorrhage
CVP readings complement clinical assessment and are not a substitute
consider advice from nursing staff
frusemide will not salvage renal function in a hypovolaemic patient the window of
opportunity for successful simple treatment is narrow
the five rules of renal failure would have helped in the management of this patient.

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ACUTE RENAL FAILURE These criteria should be applied in the context

DEFINITION
Acute renal failure is a biochemical diagnosis
defined as an acute increase in serum creatinine
resulting from injury or an inability to excrete
the nitrogenous and other waste products of
metabolism.
There are over 20 different classifications of
acute renal failure the Acute Kidney Injury (AKI)
classification is the system currently in vogue.
AKI is recognised as one of three clinical scenarios:
of the clinical presentation and following adequate
fluid resuscitation and exclusion of obstruction.
There are three stages of AKI based on GFR and
urine output, detailed in Table 9.1.
EPIDEMIOLOGY
The incidence of ARF very much depends on the
population being studied, from 5% of general
acute hospital admissions, to 10% of unplanned
surgical admissions to ICU and 50% of those with
septic shock.

1. An abrupt (within 48 h) reduction in AETIOLOGY

kidney function defined as an absolute
increase in serum creatinine level of
 26.4 mmol/l (0.3 mg/dl), or
2. A percentage increase in serum creatinine
level of  50% (1.5-fold from baseline), or
3. A reduction in urine output (documented
oliguria of < 0.5 ml/kg/h for > 6 h).
There are a diverse number of causes of ARF,
most usefully classified as pre-renal, intrinsic
renal and post-renal (Table 9.2). In surgical
patients, pre-renal failure is the most common
aetiology (75%), followed by intrinsic renal and
post-renal (20% and 5%, respectively).

TABLE 9.1

THE STAGES OF THE ACUTE KIDNEY INJURY CLASSIFICATION

Stage GFR criteria Urine output criteria

1 Increase in creatinine > 26.4 mol/l or 1.52.0-fold from baseline < 0.5 ml/kg/h over 6 h
2 Increase in creatinine 23-fold from baseline < 0.5ml/kg/h over 12 h
3 Increase in creatinine 3-fold from baseline or serum creatinine < 0.3ml/kg/h over 24 h
> 354 mmol/l

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
TABLE 9.2
COMMON CAUSES OF ACUTE
RENAL FAILURE
Pre-renal
Hypovolaemia
Sepsis
Low cardiac output
Intrinsic renal
Acute tubular necrosis
Ischaemic injury hypoxia, hypoperfusion
Nephrotoxic injury endotoxins, drugs,
contrast, pigments
Abdominal compartment syndrome
Hepatorenal syndrome
Post-renal
Bladder outflow obstruction
Bilateral ureteric obstruction
In pre-renal failure, the kidney is structurally
and functionally intact but has reduced blood
flow, hence GFR. Essentially, this is a reversible
state if acted upon urgently but may progress to
acute tubular necrosis (ATN) in hours. Intrinsic
renal failure involves parenchymal damage.
The renal vasculature, glomerular and
tubulo-interstitium may all be affected. ATN is
by far the commonest cause, which results from
a combination of ischaemic and nephrotoxic
injury. Post-renal failure results from obstruction
and back pressure which disturbs tubular func-
tion. Relief of obstruction enables urine to flow
but tubular function may be disturbed during the
recovery period.
MANAGEMENT OF RENAL FAILURE
In surgical patients, there are four common
scenarios regarding renal failure:
an elective patient at risk of renal failure
(with or without pre-operative chronic renal
impairment)
acute renal impairment in a critically ill patient
a patient with established renal failure
a patient with chronic renal failure (CRF).
PRE-OPERATIVE MANAGEMENT
AND PREVENTION OF RENAL FAILURE
Predict and protect
It is essential to identify those at risk of developing
peri-operative renal dysfunction, particularly
those with pre-existing renal impairment.
Common causes of CRF include: hypertension,
diabetes, renal artery stenosis, glomerulonephritis
and use of drugs (e.g. diuretics, ACE inhibitors,
NSAIDs, aminoglycosides).
For elective procedures, it is sometimes prudent to
delay surgery, investigate the cause of pre-existing
renal impairment and look at measures to protect
renal function, including a review of drug therapy
and avoiding nephrotoxins such as contrast
medium. Relevant investigations may include
urinalysis, renal ultrasound and more detailed
tests of split renal function such as a MAG3 scan.
It is often worth seeking the opinion of a renal
physician at an early stage. Ensure optimum
peri-operative fluid balance and optimise the
cardiovascular status especially in terms of
volume, avoiding hypotension and hypovolaemia.
Diabetes should be closely controlled.
In the emergency setting, strict attention to
fluid balance and maintenance of optimum
cardiac output is essential with further avoidance
of renal insults including nephrotoxic drugs
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and aggressive management of any sepsis. It is MANAGEMENT OF

often a combination of factors that tip a patient
into renal failure, in particular the combination
of hypovolaemia, nephrotoxic drugs and sepsis,
rather than one specific insult. In both the elective
and emergency setting, those at risk should be
reviewed regularly.
ACUTE RENAL IMPAIRMENT
The principles of management revolve around
the systematic CCrISP assessment protocol, with
particular attention to:
recognition and correction of respiratory
and circulatory problems

CASE SCENARIO 9.2

A 45-year-old previously healthy woman presents with jaundice and cholangitis. She has a pyrexia
(38.4C) and a tachycardia (115 bpm) but is normotensive. She is treated with intravenous antibiotics
and fluids and her condition improves; an urgent ultrasound scan suggests stones in the common
bile duct. An ERCP is booked for later in the week.
The ERCP proves difficult and adequate drainage of the common bile duct is not achieved. A PTC
is scheduled for the following day but, 12 h after the ERCP, the patient becomes hypotensive and
pyrexial. The serum amylase and an abdominal radiograph are normal. Treatment is started with
oxygen, intravenous fluid challenges and the intravenous antibiotics are continued. She is transferred
to the HDU and a CVP line inserted (+10 cmH2O). The blood pressure is restored but the urine
output remains poor and by the following morning the urea is 25.7 and creatinine 229. The patient
is not on any nephrotoxic drugs.
It is clear that definitive treatment in the form of biliary drainage is needed urgently. An emergency
PTC is arranged for later the same day. The PTC is performed by a consultant radiologist with an
anaesthetist and an HDU nurse in attendance and with portable monitoring in place. Successful
biliary drainage is achieved but the patient requires several days of haemofiltration on the HDU.
She eventually makes a slow, but full, recovery, has a successful ERCP and subsequent elective
laparoscopic cholecystectomy.

LEARNING POINTS
Multiple factors often contribute to acute renal failure in surgical critical care biliary
obstruction, sepsis and hypovolaemia are a potent combination.
Patients with obstructive jaundice tend to be dehydrated and need adequate fluid therapy
and clinical monitoring.
Procedures such as ERCP and PTC can exacerbate hypovolaemia or sepsis in a number of ways
and adequate peri-procedural antibiotics and intravenous fluids are needed in such cases
they are easily overlooked.
Timely, definitive treatment of the underlying cause is usually the key to success.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
immediate identification and management
of any life-threatening consequences of renal
impairment
exclusion of urinary tract obstruction if anuric
careful search for, and correction of, the
underlying cause
help early from appropriate specialists.
PRACTICE POINT
Complete anuria means lower urinary
tract/catheter obstruction until proven
otherwise.
PATIENT ASSESSMENT
An accurate history is essential, supplemented
by any information available from relatives, the
patients GP and the case notes. A note should be
made of any factors that predispose the patient
to increased risk of renal failure.
Frequently, there are no specific symptoms
associated directly with ARF. Uraemic symptoms,
commonly seen in chronic renal failure (such as
anorexia, nausea, vomiting and itching) are rare.
Signs may relate to the uraemic state particularly
related to fluid overload and pulmonary oedema,
but this may be attributed to other clinical
problems especially in the multi-organ failure
patient. A thorough, systematic examination is
essential to identify any subtle signs of underlying
disease, such as skin lesions in vasculitis, enlarged
prostate and/or bladder and polycystic kidneys.
A thorough and repeated assessment of
intravascular volume should be performed.
This can be difficult in the critically ill patient,
128
who may have adequate or excessive fluid but
in the wrong compartment. The signs of
hypovolaemia should be revised but remember
that hypovolaemia can exist in the presence
of normotension and significant extravascular
oedema. Fluid overload may lead to an elevated
blood pressure but, in particular, a raised
JVP/CVP. Extravascular fluid overload may
manifest as peripheral and pulmonary oedema,
ascites and effusions.
INVESTIGATIONS IN ARF
Dipstick urinalysis is mandatory in renal
dysfunction. Marked proteinuria or microscopic
haematuria with casts suggest a primary renal
insult. Urine biochemistry and microbiology
should also be considered, with biochemistry
sometimes helping to distinguish between
pre-renal and intrinsic renal failure (see below).
A renal ultrasound scan is also mandatory in
any patient with ARF. This should be performed
immediately in an anuric patient, if an obvious
urinary tract obstruction is not detected clinically.
Ultrasound will also provide information
regarding renal size and blood flow.
Plain abdominal X-ray is rarely useful, but plain
chest X-ray can reveal pulmonary oedema.
Further radiological investigation should only
be ordered after discussion with seniors, as it
will often entail a contrast load and further renal
insult. CT is the most useful investigation along
with radionucleotide studies in terms of identifying
problems with renal blood flow, renal function
and obstruction.
A number of blood tests should be considered to
complement routine biochemistry depending on
the clinical scenario (Table 9.3).

TABLE 9.3
BLOOD TESTS TO COMPLEMENT
ROUTINE BIOCHEMICAL ANALYSIS
FBC: to detect anaemia, infection
Routine biochemistry: urea, creatinine; check
potassium
LFT: to recognise hepatorenal syndrome
Calcium phosphate: if associated malignancy,
rhabdomyolysis or tumour lysis suspected
Creatine kinase: to detect rhabdomyolysis
C-reactive protein: as a measure of infection
and/or inflammation
ABG and lactate: to assess hypoxia, acidosis
and tissue/organ ischaemia
TREATMENT
Look for a reversible cause and act urgently to:
restore and maintain renal perfusion
relieve any obstruction
oxygenate the tubules
remove/avoid toxins
identify and treat any underlying cause.
CHECKLIST
Is it pre-renal failure?
Consider the clinical scenario. Surgical patients often
become hypovolaemic, for a variety of reasons.
Often, oliguria can be corrected by restoring volume.
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CHAPTER 9 | RENAL FAILURE, PREVENTION AND MANAGEMENT
Distinguish pre-renal from intrinsic renal failure
due to ATN
Classically, in pre-renal failure, the concentrating
ability of the tubular system is retained producing
urine with high osmolarity, high urea and creatinine
and low sodium concentration. In ATN, a low
osmolar urine with high sodium and low urea/
creatinine is produced (Table 9.4 overleaf). Note
there are many confounding variables and, in
clinical practice, the full biochemical analysis is
rarely performed.
Restore renal perfusion with volume
Aim to restore euvolaemia using 0.9% NaCl
initially, and ensure regular monitoring of cardio-
vascular parameters, particularly urine output.
Once euvolaemic, give maintenance fluid to match
urine output plus 30 ml and on going loss per
hour. If there is no rapid response to restoration
of circulating volume, central venous monitoring
is required, probably with invasive circulatory
monitoring and inotropic support.
There is no evidence to support the use of diuretics
or dopamine in the prevention or treatment of
renal impairment.
Exclude post-renal obstruction
Exclude post-renal obstruction with ultrasonography
and treat accordingly.
Distinguish between acute and chronic
renal problems
Ultrasound may reveal small kidneys (< 9 cm)
with echo-bright parenchyma, suggesting chronic
damage. The acutely injured, but normal, kidney
will be echo bright due to oedema, but normal
size and is more likely to recover. Acute or chronic
renal failure is much less likely to recover.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

TABLE 9.4

URINE VALUES IN PRE-RENAL AND INTRINSIC RENAL FAILURE

Investigation Pre-renal Intrinsic renal

Urinary specific gravity > 1.020 < 1.010
Urinary sodium (mmol/l) 1020 > 20
Urinary osmolality (mosmol/l) > 500 < 350
Urine/plasma osmolality ratio >2 < 1.1
Urine/plasma urea ratio > 20 < 10
Urine/plasma creatinine ratio > 40 < 20
Fractional sodium excretion < 1% > 1%
Renal failure index <1 >1

Note that: fractional sodium excretion = (urine/plasma sodium ratio)/(urine/plasma creatinine ratio) x 100,
and renal failure index = (urine sodium)/(urine/plasma creatinine ratio).

Oxygenate the tubules
Give oxygen and maintain a saturation of greater
than 95%. Also ensure that the Hb is greater than
7 g/dl.
Exclude toxins
Review the drug chart and avoid nephrotoxins
including contrast medium. Common examples
are aminoglycosides, NSAIDs, ACE inhibitors,
opioids and -blockers. Any drug excreted by
the kidney must have its dose altered when renal
function is impaired to prevent toxic side effects.
If in doubt, ask a pharmacist. Remember to test
for pigments such as myoglobinuria and
haemoglobinuria where appropriate.
Rhabdomyolysis is the breakdown of damaged
muscle with release of myoglobin into the
circulation. This commonly occurs following
crush injuries and following acute limb ischaemia.
Myoglobinuria is recognised as dark brown urine,
which tests positive for myoglobin on urinalysis.
Treatment includes aggressive volume expansion
and sodium bicarbonate to alkalanise the urine,
creating a diuresis and limiting the deleterious
effect of acid breakdown products of myoglobin on
renal tubules. This is only successful if recognised
early and treated immediately.
MANAGEMENT OF ESTABLISHED ARF
INDICATIONS FOR DIALYSIS
If acute renal insufficiency fails to respond to
the above measures and progresses to acute renal
failure, renal replacement therapy (RRT) will be
required. The indications for RRT are summarised
in Table 9.5.

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HAEMOFILTRATION
TABLE 9.5 In haemofiltration, there is a continuous
convection of molecules across a permeable
INDICATIONS FOR RENAL REPLACEMENT
membrane (Fig. 9.b). The fluid that is removed is
THERAPY
replaced with a buffered physiological solution.
Absolute This is more effective in removing large quantities
Refractory hyperkalaemia (> 6 mmol/l) of fluid, but not as effective as dialysis at clearing
Refractory pulmonary oedema and fluid smaller molecules. As with dialysis, filtration is
overload usually performed using a continuous veno-venous
Uraemic encephalopathy method (CVVH). This method provides the least
Relative risk of significant intravascular fluid shifts and
Acidosis (pH < 7.2) haemodynamic instability.
Uraemia
Pericarditis
Blood
Toxin removal
flow

Note that the threshold for RRT in uraemia is

controversial and relates to the rapidity of rise as
well as the absolute level of urea. A rise above 35 Dialystate
mmol/l unresponsive to other therapies is usually flow
an absolute indication. RRT can be performed by
dialysis or haemofiltration, depending on the Figure 9.3a Dialysis
clinical circumstances.

HAEMODIALYSIS Semipermeable membrane

Haemodialysis is a process by which low molecular Concentration of solute
weight solute equilibrates between a blood
compartment and a dialysate compartment separated
by a semipermeable membrane. Solute waste Replacement
moves across the membrane down a concentration fluid
Blood
gradient (Fig. 9.3a). The dialysate contains normal flow
solute, including sodium, calcium, magnesium
and chloride in the appropriate concentration to
maintain normal blood concentrations. Dialysis
can be intermittent or continuous. Intermittent
dialysis creates rapid changes in plasma osmolality Filtrate
and volume, making continuous methods more
favourable in critically ill patients. Figure 9.3b Haemofiltration

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MANAGEMENT OF An ECG should be performed. Hyperkalaemia may

LIFE-THREATENING COMPLICATIONS
HYPERKALAEMIA
Acute hyperkalaemia (K+ above 6.5 mmol/l)
requires immediate treatment to prevent life-
threatening cardiac dysrhythmia and VF/asystolic
arrest. Rate of rise is also important: a rapid rise
to 6 mmol/l is equally a cause for concern. There
are usually no symptoms specific to a rise in
potassium and clinical suspicion in the vulnerable
patient is crucial.
Any underlying contributing cause should be
identified and stopped, including blood transfusions,
drugs that reduce renal potassium excretion
(potassium sparing diuretics, ACE inhibitors, etc.),
intravenous fluid containing potassium and
potassium supplements.
cause peaked T waves, absent P waves, widened
QRS and ventricular arrhythmias. In the presence
of ECG changes and a potassium above 6 mmol/l,
emergency measures should be instituted to
+
reduce K levels temporarily, though this will only
shift the potassium into the intracellular space.
Immediate measures include (also see Table 9.6):
commencing continuous cardiac monitoring
insulin (1020 units actrapid) in 100 ml 20%
dextrose intravenously over 30 min
sodium bicarbonate 50 mmol intravenously
over 510 min
10% calcium gluconate intravenously
(1030 ml)
Beta-2 agonist, e.g. nebulised or intravenous
salbutamol.

TABLE 9.6

EMERGENCY THERAPY FOR HYPERKALAEMIA

Drug Mechanism of action Pros and cons

Calcium gluconate (i.v. 1030
ml of 10% solution)
Insulin/dextrose (insulin
[1020 U actrapid] in 100 ml
20% dextrose i.v. over 30 min)
Sodium bicarbonate (50 mmol
i.v. over 510 min followed
by i.v. infusion of 1.26% or
1.4% solution at 100 ml/h)
Salbutamol (510 g/min
by intravenous infusion, or
nebulised)
Membrane stabilisation
Drives potassium into cells
Transfer of potassium into
cells by exchange for hydrogen
across membrane
Transfer of potassium into cells
Rapid effect but transient
action
Rapid effect, intermediate
action but needs central line
Rapid effect intermediate
action, best with metabolic
acidosis; beware sodium
overload
Rapid effect, short action;
risk of tachycardia, vasodilator
effect

132

If, after emergency treatment, renal function is
not improving, treatment should be introduced to
reduce total body potassium. This can be achieved
by: (i) dialysis (particularly if combined with fluid
overload); or (ii) ion exchange resin (in the form
of calcium resonium, 15 g 68-hourly or 30 g
rectally; this binds potassium within the gut but is
very unpleasant to take and is of limited benefit).
PULMONARY OEDEMA
Pulmonary oedema presents as acute shortness
of breath, associated with anxiety, tachycardia,
tachypnoea, cool peripheries, and wide-spread
crepitations/wheeze. If suspected, a chest X-ray
should be performed immediately (if safe to do
so). Sit the patient upright, stop all intravenous
infusions, give high-flow oxygen and monitor
saturations with a view to achieve SaO2 of greater
than 95%. Further treatment options include:
intravenous diamorphine 2.5 mg for vasodilatory
and anxiolytic effects
intravenous GTN infusion, if systolic BP is
greater than 100mmHg. Commence infusion at
2 mg/h and titrate upwards every 15 min
intravenous frusemide, 250 mg in 50 ml saline
over 1 h
review regularly
discuss higher level of support, particularly
in the presence of: oligo/anuria, continued
tachypnoea (> 30/min), signs of fatigue,
respiratory failure (PaO2 < 8 kPa, PaCO2 > 7 kPa),
acidosis (pH < 7.2).
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CHAPTER 9 | RENAL FAILURE, PREVENTION AND MANAGEMENT
CHECKLIST WHEN MAKING
A NEPHROLOGY REFERRAL
Expect to answer the following:
clinical scenario what do you think is going on?
what is the pre-morbid state?
what are the most recent creatinine, serum
potassium and ABG results?
what is the volume and cardiovascular status?
what volumes of urine are they passing?
what was the pre-insult renal function?
what does the ultrasonography show?
what drugs are they on (in particular have they
received any nephrotoxins)?
PROGNOSIS AND RECOVERY
As individual nephrons recover, the kidney
behaves as in chronic renal failure. Because only
a proportion of the nephron mass has recovered,
each nephron has a much higher solute load to
excrete. There is, therefore, a major limitation in
the kidneys ability to conserve sodium, potassium,
bicarbonate and water. With modern management
of renal failure, it is unusual to see major problems
with large fluid and electrolyte losses. The major
exception is in postobstructive diuresis where
losses need to be measured and replaced as
appropriate. It is important that the recovering
kidney is not exposed to further hypotensive or
nephrotoxic insults. By 6 months, the kidney will
normally have recovered to 8590% of pre-morbid
function, though some patients will invariably
progress to CRF requiring permanent RRT or
transplantation (10%).
Prognosis is often determined by the severity
of the underlying incident that caused the ARF.
However, in-hospital ARF due to ATN carries
2030% mortality, most commonly due to
infection or cardiovascular complications.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 9.3

You are asked to see a 75-year-old hypertensive diabetic woman on the ward who had a reversal
of Hartmanns procedure 2 days ago. Her observations reveal a BP of 110/70, pulse 100 bpm,
temperature 37.8C, O2 sats 89% (on air) and urine output of 20 ml for the past 3 hours. Her
blood tests this morning are available: Hb 10.1, Ur 8, Cr 123, Na 130, K 5.0.
WHAT ARE YOUR PRIORITIES AND WHAT OTHER INFORMATION DO YOU WANT TO KNOW?
Follow the CCrISP protocol, in particular with regard to the renal dysfunction. This lady is
unstable and needs careful monitoring. She may be developing acute renal failure.
To restore renal perfusion, you should prescribe a fluid challenge (0.9% saline 1 l over 2 h)
but you do not want her to develop pulmonary oedema.
Oxygenate the tubules by sitting the patient up, give high flow oxygen and institute continuous
O2 monitoring.
Review drugs for nephrotoxins. You stop an ACE inhibitor and NSAID.
Regular observations (every 30 min) aiming for systolic BP of 130140, BP < 100 bpm,
SaO2 > 95%, RR 1215, and urine output of 30 ml/h. Set a time for review in 12 h.
You would want to know the pre-operative blood pressure and serum creatinine, weight of the
patient, plus fluid balance since surgery.
After the fluid challenge, you find the blood pressure has improved with a systolic pressure of 140,
which is good for renal perfusion, although urine output is still poor at 20 ml in 2 h. The SaO2 is
94% on supplemental oxygen and, worryingly, the respiratory rate has risen to 24/min.
HOW WOULD YOU MANAGE THIS SITUATION NOW?
The findings suggest pulmonary oedema may be developing. Stop further fluid challenges. Perform
a fluid assessment to look for evidence of fluid overload. You arrange a chest X-ray and ABGs,
re-check U+Es.
The chest X-ray shows interstitial oedema, and ABG reveals an acidosis (pH 7.25, PaO2 9 kPa,
PaCO2 4.5, BE-5, lactate 2) and the biochemistry is worse (Ur 12, Cr 148, Na 129, K 5.9).
WHAT IS YOUR ASSESSMENT? WHAT SHOULD YOU DO?
It looks like she is now developing pulmonary oedema (interstitial oedema, hypoxaemia) and acute
renal failure (Cr and K rising, metabolic acidosis). She needs a higher level of care than the ward.
Discuss with HDU her organ failure and need for renal and respiratory support.

LEARNING POINTS
Predict and prevent renal failure by identifying the surgical patient at risk.
Immediate management of renal failure requires close attention to fluid balance while
recognising the risk of developing pulmonary oedema.
Pulmonary oedema can be life-threatening and often requires a higher level of care with
respiratory and renal support.

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 CHAPTER 9 | RENAL FAILURE, PREVENTION AND MANAGEMENT

Patients who have CRF, therefore, have much less

PRACTICE POINT ability to compensate for circulatory stress and
Acute renal failure is not a cause of death the effects of nephrotoxins. A simple example is
unless a decision has been made not to treat the patient with significant CRF (creatinine of 300
the resultant uraemia. The cause of death is mmol/l) who is fasted overnight prior to surgery.
the underlying condition. This will cause mild intravascular volume
depletion. As there are far fewer nephrons, each
has to carry increased solute and this acts as an
osmotic diuretic that prevents concentration of
FUTURE DEVELOPMENTS
the urine. This prevents maximum sodium and
Creatinine and urine output are relatively water retention until there has been a significant
insensitive markers of renal function and hence fall in glomerular filtration rate secondary to a
new biomarkers are being sought to identify and contracted circulating volume. Thus, the patient
predict those at risk of impending ARF, including becomes dehydrated and renal function diminishes
neutrophil gelatinase-associated lipocalin, and further. Depriving patients with CRF of oral fluid
kidney injury marker-1. for any significant length of time (greater than
46 h) should be avoided unless fluid is given
CHRONIC RENAL FAILURE intravenously.
CRF is defined as chronic irreversible loss of Many patients with severe CRF will be chronically
nephron mass resulting in permanent impairment anaemic. Rapid transfusion will acutely impair
of solute waste excretion. These patients are not renal function by altering the flow characteristics
necessarily requiring permanent RRT. By estimating of the blood and is seldom necessary.
the GFR using the Cockcroft Gault formula, 5%
Patients with renal transplants must be managed
of the adult population will have sub-clinical
in conjunction with their nephrologist or transplant
stage 3 CRF (a GFR 3060 ml/min). However,
centre. Skilled assistance will be required to
such patients deserve special attention to detail
manage their immunosuppression and reduce the
due to:
likelihood of an acute rejection episode.
significant risk of developing ARF
multiple medications, especially cardiovascular
drugs
concomitant silent cardiovascular disease
abnormal cardiovascular physiology
autonomic dysfunction reduces normal response
to volume changes, especially diabetics
abnormal gastrointestinal function delayed
transit, impaired absorption
abnormal drug handling impaired excretion
requires dose modification; consult with
pharmacy.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

SUMMARY
Predict and prevent renal failure, and remember
the five rules of renal dysfunction in surgical
patients:
The kidneys cannot function without
adequate perfusion.
Renal perfusion is dependent on adequate
blood pressure.
A surgical patient with poor urine output
usually requires more fluid.
Absolute anuria is usually due to urinary
tract obstruction.
Poor urine output in a surgical patient is not
a frusemide deficiency.

FURTHER READING
Acute Renal Failure
Hilton R. Acute renal failure. BMJ 2006;
333: 78690.
Mehta RL, Kellum JA, Shah SV et al.
Acute Kidney Injury Network: report of an
initiative to improve outcomes in acute kidney
injury. Crit Care 2007; 11: R31.
Fluid assessment/management
Powell-Tuck J, Gosling P, Lobo DN et al.
British Consenus Guidelines on Intravenous Fluid
Therapy for Adult Surgical Patients (GIFTASUP).
London: NHS National Library of Health, 2008.
Oxford Handbook of Nephrology and Hypertension.
Oxford University Press, 2006.

136
10
Peri-operative
management of
the surgical site

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
recognise the difficulties of assessing the
surgical patient postoperatively, especially
on the ICU
understand how the CCrISP system can
be utilised to assess and manage problems
associated with the surgical site effectively
be aware of the presentation of common
and/or serious complications in surgical
patients and develop an approach to both
their prevention and treatment
develop an approach to the management
of the surgical sites in the form of wounds,
drains and stomas.
INTRODUCTION
Surgery is a significant physiological insult,
especially when performed for a critical presentation.
The time following the procedure requires a plan
of resuscitation and recovery in successful cases,
but there is always a risk that complications
may arise, including infection, haemorrhage,
ischaemia or incomplete resolution of the original
presentation. The challenge is to be able to
recognise any deterioration early and intervene
before the advent of organ failure and subsequent
ICU requirement with its inherent high mortality
risk. While recognising a deterioration in the
immediate management, the history of the
presentation or the operation notes may give
a better guide to a likely cause, or allow successful
intervention if events are predicted. The anticipation
of problems is a great skill to acquire (see Table
10.1), allowing earlier and targeted intervention
138
to decrease the chance of deterioration.
Significant deterioration may require ICU
admission for resuscitation and monitoring;
if organ failure ensures, the operative mortality
can be in excess of 50%.
Whether on the ward or in a higher dependency
area it is often difficult to assess the surgical site,
especially within the abdomen. However, it is the
surgical teams responsibility to ensure that there
is appropriate monitoring and a management
plan. This includes all components of the surgical
site, including wound management and plans for
drains, stomas or fistulae.
PRACTICE POINT
TASK: reflect on your last major operation.
Consider what the potential complications were,
and how these may present. If the patient did
experience complications, were there things
that could have been done to prevent these?
POSTOPERATIVE ASSESSMENT
OF THE SURGICAL SITE
The end of an operation is equivalent to the
decide and plan component of the CCrISP
assessment system. The desired expectation would
be for the patient to be stable and progressing
safely within a structured management plan.
That plan begins with the operation note where
the indication for the procedure, especially if in
a critical pre-operative condition, and the
essential findings should be clearly documented.
The operative procedure and any difficulties
encountered should be described. An operative
diagram is often helpful to describe the internal
and external anatomy, as well as representing
 CHAPTER 10 | PERI-OPERATIVE MANAGEMENT OF THE SURGICAL SITE
TABLE 10.1
EXAMPLES OF ANTICIPATED POSTOPERATIVE COMPLICATIONS
ASSOCIATED WITH INITIAL PRESENTATION
Surgical presentation
Infarcted bowel from intestinal ischaemia
Ruptured abdominal aortic aneurysm
Diverticular abscess and systemic sepsis
Penetrating abdominal trauma
Appendicitis
Any presentation with co-morbid risk factors:
age, obesity, smoking and diabetes
the position of drains and stomas. Clear
postoperative instructions must be written
especially with regard to the management of
drains or stomas and when or how to start
feeding (see Case Scenario 10.1).
139
Potential postoperative complication
Further ischaemia causing anastomotic
breakdown, abscess/collection, fistula formation
Open repair: reactive or secondary
haemorrhage/abdominal compartment syndrome/
lower limb ischaemia/postoperative ileus
Endovascular repair: stent thrombosis and limb
ischaemia/abdominal compartment syndrome/
renal impairment
Anastomotic leak and recurrent sepsis
Intra-peritoneal abscess
Any inotropic support will increase risk of
anastomotic leak or end stoma infarction
Increased risk of sepsis/need for laparostomy
if regular re-look laparotomy required
Risk of abdominal compartment syndrome
Wound infection and abscess formation
Intra-peritoneal pelvic collection
Task: consider these co-morbidities and the
complications which might occur related to
these factors. Then refer to Chapter 16 for
further information
Also, a description of anticipated complications
or the warning signs, that need prompt surgical
review at an appropriate level, will prevent delay
in the identification of deterioration, especially
if on ICU.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
When you are asked to assess the postoperative
patient, it is likely that they are deviating from
their predicted course. From your knowledge of
the pre-operative presentation, such as the
examples in Table 10.1, you should have suspicions
of potential complications. However, you must
always use the CCrISP system of assessment to
guide your management and prevent omissions.
Even if you are unsure of the cause, the system
will enable you to recognise whether the patient
is unstable and/or deteriorating, and that the patient
may require senior surgical or ICU assessment.
Call for help early, but continue your systematic
process of assessment and resuscitation.
ANTICIPATING A NEED FOR ICU
You know that some patients are planned for
ICU pre-operatively because of factors that predict
a likely need for more intensive support, such as:
their age
critical nature of their diagnosis
pre-operative co-morbidity
acute physiological stress.
These prophylactic transfers to a higher level
of monitoring allow for early recognition of
any complication and so minimise the delay
in treatment. Likewise, any of these factors in
a deteriorating surgical patient on the ward
should prompt earlier transfer to ICU.
RECOGNISING DETERIORATION ON ICU
The benefit of more intensive monitoring is the
early recognition of systemic changes since these,
rather than the examination of the abdomen or
chest, are far more accurate signs of deterioration.
A colonic anastomotic leak should cause peritonism
and distension but, if a patient is still paralysed
and ventilated, these will be masked. It is more
likely that subtle physiological changes such as
140
increasing oxygen or ventilatory requirement
will raise a suspicion in such patients.
While the abdomen may seem a likely source
when deterioration occurs after laparotomy,
consider alternative causes such as sepsis from
lines, urine or chest, or limb ischaemia in a
prothrombotic state.
However, remember that, once on ICU, the patient
has little physiological reserve and a missed intra-
abdominal sepsis or ischaemia is often fatal!
ASSESSING THE ABDOMEN ON ICU
PRACTICE POINT
Consider previous ICU patients you have seen
with abdominal pathology. Were there obvious
abdominal signs or did you rely on the charts
to identify clinical deterioration?
Often clinical signs on the ventilated patient can
be very subtle and even misleading. It is easy
to be lured into a false sense of security because
the abdomen feels soft and non-distended. The
charts will guide you towards recognising the
problem. It may be a gradual increase in oxygen
or ventilatory requirements, or an increasing
dependence in inotropes to maintain perfusion.
The urine output may be gradually diminishing
despite adequate fluid filling.
PRACTICE POINT
Think of patients you have seen that have
demonstrated these features. Was there a
concern about re-operating, or a delay in
return to theatre?
 CHAPTER 10 | PERI-OPERATIVE MANAGEMENT OF THE SURGICAL SITE
TABLE 10.2
WARNING SIGNS OF SIGNIFICANT PATHOLOGY
Warning sign
Neutropenia (WCC < 2000 x 109/l)
Grossly elevated WCC (> 20,00025,000 x 109/l)
Metabolic acidosis
Often, due to the subtle and gradual clinical
deterioration, there are delays in taking patients
to theatre. While it may be the systemic signs
that herald the patients deterioration, the
diagnostic question is whether this is due to
bleeding, perforation, mesenteric ischaemia,
pancreatitis or sepsis and where the source may
be. Within the abdomen there may be temptation
to confirm the diagnosis with imaging, but one
should carefully appraise the benefits of this as
opposed to direct intervention with a laparotomy.
In the case of a suspected colonic anastomotic
leak, a CT scan and contrast enema are
complementary, with the former the investigation
of choice with the possibility of additional
percutaneous drainage. However, a negative scan
does not exclude a leak completely and the time
and delays of the transfer to and from the CT
scanner should be considered against the benefit
of rapid drainage from an immediate return to
theatre. Likewise, an ultrasound may show free
fluid but that will very rarely change your
management. Simple blood tests, particularly
141
Underlying cause
Overwhelming sepsis/profoundly impaired
host response
Sign of infarction
Also occurs post splenectomy
Consider Clostridium spp. infection if
associated diarrhoea
Tissue hypoperfusion from ischaemia or sepsis
the white cell count and blood gases, may guide
you towards a specific cause of deterioration as
shown in Table 10.2. You should also remember
to take all possible cultures (blood, pus, urine or
sputum, etc.) in order to direct therapy in the
longer term. If you are not sure, seek senior help
and advice. Dont just organise more tests!
In more subtle postoperative changes, contrast
CT arterial imaging may exclude an ischaemic
cause. Isolating a focus of infection may require
a labelled leukocyte scan. However, in acute
deterioration there is not the time to delay and
a laparotomy may be indicated.
Occasionally, negative laparotomies are performed
as part of a diagnostic process when faced with a
deteriorating surgical patient. This is not necessarily
a wrong course of action, but extended delay of
the patient who does need to return to theatre will
invariably lead to a worse outcome.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 10.1

You are asked to assess a 45-year-old, 120 kg man on the ICU who is 10 h postoperative from
a laparotomy for blunt abdominal trauma. There is concern that, despite fluid resuscitation, he
remains tachycardic and hypotensive. He is still ventilated. You arrive on the ICU and the nurse
asks: Do you think he could be bleeding?
HOW WOULD YOU MANAGE THIS SITUATION?
This is for you a difficult and complex assessment, especially since the patient remains ventilated.
However, if you follow the CCrISP system, this patient can be assessed thoroughly and systematically
in a similar manner to the non-ventilated patient (Fig. 10.1). You follow the system and your
immediate management is as follows:
A: intubated and ventilated
B: ICU report increasing airway pressure required to ventilate
C: P = 120 bpm, BP = 90/60 mmHg, CVP = 12 cmH2O, though cardiac output is reducing.
No external signs of continued haemorrhage. Minimal reduction in Hb from 9.5 to 8.6 g/dl in
the last 5 h though has had 4 unit transfusion since theatre. Urine output 200 ml in the last 7 h
D: pupils respond appropriately. Patient is paralysed
E: this patient is obese but you note that the abdomen appears distended.
IS THIS PATIENT STABLE OR UNSTABLE AND WHAT WOULD YOU DO AT THIS STAGE?
The patient is clearly unstable. You need to consider whether more resuscitation is required or whether
to call the surgical consultant for an immediate return to theatre. It is probably reasonable to gather
more information at this stage and continue with the system of assessment while the ICU staff
continue resuscitation. Using the CCrISP system, you would perform a full patient assessment. The
available results are (all conventional units): Hb 8.6, WCC 18.9, platelets 65, amylase 240, sodium 128,
potassium 5.9, urea 12.5, pH 7.3, PO2 8.5 kPa, PaCO2 6 kPa, BE 7 (increased from 3 in last 3 h).
Chart review: the operation note reports the need for a splenectomy and extensive bleeding from
the vena cava (Fig. 10.2).
DOES THIS HELP YOU MAKE A DECISION? DO YOU HAVE A DIAGNOSIS? CONSIDER
WHAT YOUR MANAGEMENT PLAN WOULD BE AND WHETHER YOU NEED ANY OTHER
INVESTIGATIONS.
You should have recognised that the intra-abdominal pressure was elevated at the time of closure and
simple investigation is to repeat the bladder pressure, which is now 28 mmHg. Therefore, this patient
has abdominal compartment syndrome and requires immediate return to theatre to re-open his

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abdomen. Further delay increases the risk of worsening organ dysfunction and further resuscitation or
conservative measures will be futile without immediate decompression. You arrange for the patient to
return to theatre and inform the surgical consultant. On laparotomy, there is no ongoing haemorrhage
and his colon is viable so the abdomen is left open as a laparostomy.
CONSIDER THE PROBLEMS THAT MIGHT BE ENCOUNTERED WHEN THE PATIENT IS
TRANSFERRED BACK TO ICU.

LEARNING POINT
Abdominal compartment syndrome can lead rapidly to multiple organ failure which, without
immediate decompression, is invariably fatal.

Immediate management
ABCDE

Full patient assessment

Chart review
History and systematic examination
Available results

Decide and plan

Stable patient Unstable/unsure

Daily Diagnosis required

management plan Specific investigations

Definitive care
Medical
Surgical
Radiological

Figure 10.1 The CCrISP system of assessment.

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Figure 10.2 Operation note.

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TABLE 10.3

SYSTEMIC EFFECTS OF ABDOMINAL COMPARTMENT SYNDROME

System Intra-abdominal pressure

1015 mmHg 1625 mmHg > 25 mmHg
Cardiovascular Reduced preload and Reduced contractility
increased afterload Gross reduction in
Reduced cardiac output cardiac output
Renal Oliguria Anuria
Gastrointestinal Slight intestinal Marked intestinal Bowel infarction
and hepatic ischaemia and hepatic ischaemia Hepatic failure
CNS Minimal effect Increased intracranial
pressure

SPECIFIC SURGICAL SITE
COMPLICATIONS
ABDOMINAL COMPARTMENT SYNDROME
Abdominal compartment syndrome or the
presence of elevated intra-abdominal pressure
is a significant cause of morbidity and mortality
among critically ill surgical and medical patients.
As shown in Table 10.3, significant systemic
effects occur with a rise in abdominal pressure.
The actual development of intra-abdominal
hypertension (IAH) is a continuum of
pathophysiological changes that begins with
a disturbance of regional blood flow and
culminates in frank end-organ failure, due to
the development of abdominal compartment
syndrome. The aetiology of IAH may be
intra-abdominal, particularly in abdominal
trauma patients (see scenario above), pancreatitis
or following aortic surgery, but can also occur
due to an extra-abdominal cause, such as
burns or sepsis associated with aggressive fluid
resuscitation.
The intra-abdominal pressure is expressed in
mmHg, with the usual level being sub-atmospheric
to 0 mmHg, though elevation to the range of 57
mmHg is common.
IAH is defined as a sustained or repeated elevation
of IAP > 12 mmHg and is graded as: I, 1215
mmHg; II, 1620 mmHg; III, 2125 mmHg; IV >
25 mmHg. Grade IV requires surgical decompression.
The cardiac effect of IAH is due to elevation
of the diaphragm and the subsequent rise in
intrathoracic pressure, which in turn reduces the
venous return and cardiac output. Such changes
are far more likely in the hypotensive patient
and so early signs of pressure elevation should
be managed by fluid resuscitation.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Intra-abdominal pressure is measured by assessing
intravesicular/bladder pressure. The measurement
should occur at the end of expiration with the
patient in the complete supine position, after
ensuring that abdominal muscle contractions are
absent. The transducer is zeroed at the level of the
mid axilliary line and connected to the bladder
catheter. Sterile saline (25 ml) is inserted into the
bladder to act as a conductive fluid column.
Abdominal compartment syndrome is the
progression of pressure induced end-organ changes
and, if due to intra-abdominal causes such as
trauma or acute pancreatitis, is characterised by
rapid deterioration which if not recognised and
treated is commonly fatal.
The expedient treatment of ACS is to re-open
or perform a laparotomy wound in order to
decompress the abdomen. As in the scenario
above, a thorough wash-out of all fluid/blood
should be performed, with a detailed inspection
for sites of bleeding. The bowel should be
carefully inspected for signs of ischaemia.
Figure 10.3 A laparostomy and outcome following mesh closure and skin graft.
146
There are a number of options available at the
end of the laparotomy though, almost invariably,
primary closure should not be considered.
A large saline infusion bag can be opened up
and sutured to the fascial edges in order to
provide a temporary seal of the abdominal cavity.
Specific bowel bags can also be used in a similar
way. This may later be converted to a mesh
covered with packs or a negative pressure dressing.
There is some concern that negative pressure
can encourage the formation of a fistula from
oedematous and friable bowel. Fig. 10.3 shows a
laparostomy in a patient who later underwent
successful split skin graft closure.
Postoperatively, laparostomy patients can be
challenging for ICU staff to manage, particularly
from the nursing point of view. The surgical staff
should liaise closely with the ICU staff and predict
problems with fluid and temperature losses through
the laparostomy wound, the potential for sepsis
especially with respect to any underlying vascular
grafts, and make a plan to achieve wound closure.
 CHAPTER 10 | PERI-OPERATIVE MANAGEMENT OF THE SURGICAL SITE

CASE SCENARIO 10.2

You are asked by the ICU staff to assess a 25-year-old man who, 14 h following laparotomy for
a penetrating abdominal stab wound, is becoming increasingly unstable with a BE of 8. You follow
the CCrISP system to assess and resuscitate the patient systematically. Your findings from the initial
management are:
A: intubated
B: ventilated
C: P = 120 bpm; BP = 95/75; CVP = 6 cmH2O, cold peripheries, pedal pulses not palpable,
requiring increasing dose of noradrenaline, urine output 250 ml since return from theatre
D: pupils respond appropriately. Patient is paralysed
E: abdominal wound is laparostomy, with appearance of right-sided stoma.
Full patient assessment of available results: Hb 9.0, WCC 24, platelets 75, amylase 200, sodium
130, potassium 6.5, urea 16, pH 7.2, PO2 18.5 kPa, PaCO2 5 kPa, BE 8, lactate 5, CK 4000 u/l.
Chart review showed the patient was stabbed in the abdomen after an evening out drinking and
suffered significant blood loss at the scene. He had a systolic pressure of only 70 mmHg on arrival
in A&E. He was immediately taken to theatre, where laparotomy findings were a distal aortic
laceration and a small sigmoid laceration with minimal contamination. The sigmoid laceration
was closed primarily but defunctioning ileostomy performed. Significant blood loss occurred before
and during the aortic repair with repeated episodes of clamping. It was a long procedure; therefore,
abdominal packing was inserted with a re-look planned at 24 h.
WHAT DO YOU THINK MIGHT ACCOUNT FOR THE DETERIORATION AND HOW WOULD
YOU MANAGE THE SITUATION?
It is unlikely to be abdominal compartment syndrome because of the laparostomy. You need to
perform a thorough systematic examination, in particular looking at his lower limb vasculature
because of the history of aortic injury. Only femoral pulses are palpable; both feet are cold and
poorly perfused. From toes to knees, the calves are very swollen and tense. The patient is clearly
unstable and requires no further investigations to confirm the diagnosis of bilateral lower limb
compartment syndrome. Arrangements are made for urgent fasciotomies to be performed. Upon
performing the fasciotomies, all muscle groups are very oedematous and immediately bulge from
the wounds. Some areas of muscle do not contract to electrical (diathermy) or physical stimuli,
though other areas contract normally.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
LOWER LIMB COMPARTMENT SYNDROME
Limb compartment syndrome should always
be considered when there has been a period of
ischaemia and perfusion. Case Scenario 10.2
highlights the need for thorough systematic
assessment and prompt therapeutic action. A delay
in recognising limb compartment syndrome can
rapidly lead to irreversible muscle damage resulting
in permanent neuromuscular defects within 12
hours. This may necessitate amputations. Also,
aggressive fluid resuscitation is required to
minimise the effects of myoglobin from muscle
breakdown that can cause renal failure.
Lower limb trauma and associated hypotension
may lead to re-perfusion with significant rises in
interstitial pressure and subsequent compartment
syndrome. Beware also a prolonged operation in
the lithotomy position; this can also produce
compartment syndrome and, any delay in treatment,
minimises the chances of limb salvage. If there
was any doubt in the diagnosis, compartment
pressures can be performed with a needle inserted
into each compartment, with the knowledge that
tissue necrosis can occur with an interstitial
pressure as low as 30 mmHg.
PRACTICE POINT
An old surgical word-of-mouth adage is
that if you are thinking of the need for
fasciotomies, then you should perform them
without further discussion!
COMPARTMENTS TO DECOMPRESS
The lateral compartment/superficial posterior/deep
posterior and anterior compartments of the leg
all require decompression and this should be
performed in a sterile environment in theatre.
148
After the procedure there will, due to the muscle
oedema, be a lot of fluid discharge from the
wounds. It is important that instructions for
dressing are clear and that no compression should
be applied to reduce blood or fluid loss from the
wounds. Occasionally, brisk venous bleeding can
occur from the wounds that may require further
surgical exploration to control the source.
Compartment syndrome can also occur in the
thigh and upper limb and the management
principles are identical.
BURST ABDOMEN
This complication is at the other end of the
spectrum from compartment syndrome though
the immediate management is similar to a
laparostomy with the aim to keep the exposed
viscera warm and moist and minimise the loss
of fluid and temperature. It now occurs rarely,
since the advent of mass closure with synthetic
monofilament sutures. When it does occur, the
pink sign, of serosanguinous discharge some
810 days after the initial surgery, usually heralds
it. If there were little systemic upset, the abdomen
should be resutured within 34 hours; however, if
there is systemic instability, it would be better to
manage the wound as a laparostomy temporarily.
POSTOPERATIVE BLEEDING
Despite anticipating bleeding problems, postoperative
haemorrhage can be covert with the only signs
manifesting in progressive haemodynamic
deterioration. An example would be after an
angiogram with a high puncture of the common
femoral artery, when a retroperitoneal bleed
is not uncommon. The ability to predict this
complication should be high, providing the
ability to react early with surgical correction.
 CHAPTER 10 | PERI-OPERATIVE MANAGEMENT OF THE SURGICAL SITE

Primary haemorrhage occurs at the time of surgery.
If difficult to control particularly if from the liver,
pelvis or other inaccessible sites consideration
should be given to packing the effected area with
a view to return to theatre at 48 hours for removal
of packs and re-inspection of the operative site.
A reactive haemorrhage is generally due to a
technical failure such as a slipped ligature, which
may present itself while the patient is in recovery
or having returned to the ward from theatre.
Again, this requires a thorough systematic
assessment to ensure prompt detection and return
to theatre. Examples where this might occur
include after splenectomy due to a short gastric
ligature coming loose. Even though the vessels
are small, this bleed can still cause a rapid
deterioration and cardiovascular compromise.
Reactive haemorrhage may also occur after fluid
resuscitation in trauma patients when the
increased perfusion pressure may initiate bleeding.

CASE SCENARIO 10.2 CONTINUED

You are asked to re-assess the patient from Case Scenario 10.2, 4 h after the returning to ICU, with
blood staining of the laparostomy bag and a 2.5 g/dl fall in Hb (now 6.5 g/dl compared to 9 g/dl
at the time of leaving theatre).
HOW WOULD YOU MANAGE THIS SITUATION?
This is often a difficult balance between a decision to return to theatre and control of coagulopathy.
This decision should be made in collaboration with the ICU staff. There are a number of factors
that will predispose to coagulopathy, including the massive blood transfusion, hypothermia and
reperfusion injury.

LEARNING POINT
A coagulopathy is common in critically ill patients and should be considered as a cause of any
overt or concealed haemorrhage. Any clotting problem should ideally be corrected prior to
re-operation, and this may require close collaboration between surgeon, anaesthetist and
haematology staff. Be careful not to ascribe surgical bleeding to a general bleed associated with
a minor coagulopathy, as trying to correct the clotting will not improve the situation. Indeed,
further delay may cause worsening of the coagulopathy and a cycle of deterioration. It is better
to control the specific source and correct the coagulopathy in theatre.
Other factors to consider with generalised bleeding problems are:
effect of anticoagulant therapy
a recent large transfusion
the presence of sepsis or DIC
previously unrecognised concomitant bleeding disorders, either congenital
(e.g. Waldenstrms macroglobulinaemia) or acquired e.g. drugs).

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Secondary haemorrhage occurs much later, often
78 days following a procedure. It is often related
to infective complications but still may be
unexpected and unheralded; control may be
difficult to achieve. More proximal vascular
control is often required and should be considered
at the time of re-operation.
PRACTICE POINT
Reversing a coagulopathy will not stop
surgical bleeding. Correct the coagulopathy
while addressing the source of the bleeding.
NECROTISING FASCIITIS
Necrotising infection can be difficult to diagnose;
early diagnosis and targeted treatment is essential.
Any diagnostic delay increases the mortality, which
has a range of 2573%. Immunocompromised
patients on chemotherapy or steroids are vulnerable,
but diabetes is the leading predisposing factor.
The causative bacteria are synergistic and cause
an infection involving the subcutaneous fascial
layer, inducing extensive undermining of
surrounding tissues. Presentation may be primary,
where no portal of entry or causative factor is
found, or secondary, due to a precipitating event
such as a peri-anal abscess.
The initial features may be subtle including
influenza-like symptoms and localised discomfort
or pain. Subsequently, the limb or painful area
begins to swell and may show a purplish rash.
The skin marking will then blister with blackish
150
fluid, and patients undergo severe systemic
collapse due to sepsis. The treatment required is
prompt, aggressive debridement, with wide
excision of all involved tissue back to bleeding
edges. This may be quite extensive, and can take
more than one operation. Patients usually require
systemic support along with broad-spectrum
antibiotics.
ANASTOMOTIC LEAKAGE
The typical signs of anastomotic leakage are of
systemic instability with abdominal pain and/or
rigid abdomen, tachycardia and fever. However,
there may be a far more insidious presentation
with low-grade fever, a prolonged ileus or failure
to thrive. Therefore, anastomotic leakage should
be considered as a cause for any unexplained
postoperative deterioration following bowel surgery.
This is particularly the case for laparoscopic
colonic surgery, where there may be a reluctance
to re-operate on vague clinical signs. Leak rates
for laparoscopic colonic surgery range from 2.512%
in the literature. While less likely, it should be
recognised that a defunctioning stoma does not
exclude the possibility of an anastomotic leak.
In trying to anticipate anastomotic leakage,
it is important to review the notes and the charts.
For example, does the anaesthetic chart indicate
pre-operative dehydration or any episodes of
peri-operative hypotension? Does the operation
note comment on the quality of perfusion in the
mesenteric vessels? In an emergency case, does
the ICU chart show that inotropes were required,
that may have caused mesenteric vasoconstriction?
Factors that predispose to leak are shown in
Table 10.4.
 CHAPTER 10 | PERI-OPERATIVE MANAGEMENT OF THE SURGICAL SITE
TABLE 10.4
RISK FACTORS FOR INTESTINAL
ANASTOMOTIC LEAKAGE
Anastomotic technique
Tension, poor anatomical blood supply
(particularly after anterior resection),
unrecognised mesenteric vessel damage,
poor suture technique (eversion or mismatch)
Local factors
Obstruction, ischaemia or peritonitis
Systemic factors
Shock (excessive bowel preparation or
excessive blood loss), age, malnutrition,
immunosuppression
In trying to make the diagnosis of a leak, a CT scan
and contrast enema may have a complementary
role, though the CT scan with contrast is the likely
radiological procedure of choice. If a collection is
shown to indicate a localised leak, a CT- or
ultrasound-guided drainage may be indicated.
However, major leakage has a significant mortality
(1015%) and so prompt re-operation is indicated
with exteriorisation of suitable ends of small and
large bowel. At this time, the need for nutritional
support and the potential routes of access should
be considered.
It is important to anticipate the difficulty of
re-operative surgery on ICU patients and follow
the principles shown in Table 10.5. A senior
surgeon should be involved early in the decision
making, and certainly in the surgery.
151
TABLE 10.5
PRINCIPLES OF RE-OPERATIVE SURGERY
FOR ABDOMINAL SEPSIS
Prepare the patient as well as is reasonably
possible
Anticipate the difficulty of re-operative
surgery and involve a senior surgeon
Aim to deal with the source of the primary
problem definitively
Exteriorise leaking bowel
Remove dead tissue
Culture pus and drain sepsis
Consider gastrostomy or jejunostomy for
ease of future management
THE MANAGEMENT
OF INTESTINAL FISTULAE
The evolution of an abdominal wall intestinal
fistula provides significant management
challenges, which are likely to require high
dependency care even if there is no complicating
infection or sepsis. The management involves the
monitoring of significant fluid and electrolyte
losses and their subsequent replacement along
with nutritional therapy. Also involved is the
physical management of the fistula; the
surrounding skin requires protection by dressings
or bags, and this will require the input of the
stoma therapist.
When a fistula occurs postoperatively, assess by
the CCrISP protocol and then utilise the SNAP
(sepsis, nutrition, anatomy, procedure) protocol.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

S Sepsis Obtain adequate drainage

May involve CT-guided or surgical drainage
May involve defunctioning of the bowel
N Nutrition Provide nutritional support
Often this will be parenteral
A Anatomy Delineate using imaging the site of leak
CT with contrast is preferred choice
P Procedure Ultimately aim for reparative procedure
Delay until patient is well enough to predict success (this may be months)

CASE SCENARIO 10.3

Consider the surgical case from Case Scenario 10.1, in which the patient developed a compartment
syndrome and required an urgent laparotomy. The abdomen was washed out and closed primarily
at 48 h with a large bore drain inserted via the left iliac fossa along the paracolic gutter into the
splenic bed. The drain produces 50 ml of haemoserous fluid for 48 h; however, before it can be
removed, suddenly drains 300 ml of similar fluid.
HOW WOULD YOU MANAGE THE PATIENT? COULD THIS BE A FISTULA AND IF SO
WHAT IS THE POTENTIAL SOURCE?
As always, use the CCrISP system with simultaneous assessment and resuscitation. Following
immediate management, you decide that the patient is stable and proceed to the full patient
assessment. On review of the operation note, you should note the gastric repair and the splenectomy,
and consider a missed injury to the pancreas or small bowel, or a leak from the gastric repair.
A pancreatic fistula (remember to send the draining fluid for an amylase level) may give further
problems due to the digestive actions of the pancreatic fluid, with concern for the various sites of
surgical repair. A high small bowel fistula can cause high volume losses of fluids and electrolytes
and rapid changes to acidbase balance. These are complex problems and it is important to
recognise them early. A diagnosis is essential and, while testing the fluid for amylase may suggest
a pancreatic fistula, further radiological investigation is likely to be required, including contrast-
enhanced CT. Having made a diagnosis, the SNAP protocol should be used to manage the patient
further. Specialist, senior help should be enlisted for the management of intestinal fistulae.

152
 CHAPTER 10 | PERI-OPERATIVE MANAGEMENT OF THE SURGICAL SITE
MANAGEMENT OF STOMAS AND DRAINS
There are various stomas that may form a part of
the postoperative management of patients. Both
on the ward and critical care areas, this should be
directed by the surgical team with the support of
the stoma care nurse, or nutritional support team
in the case of feeding stomas.
FEEDING GASTROSTOMY OR JEJUNOSTOMY
The timing, content and volume of nutritional
support should be planned according to bowel
function with the surgical team liaising with
the dietician or nutritional support team
(see Chapter 13).
There must be clear advice given on timing of
removal and obvious marking of the feeding
stoma to prevent accidental removal if mistaken
for a drain. Ten days is usually the minimum
time allowed for a suitable seal to form.
a)
b)
Figure 10.4 a) End colostomy, and b) loop ileostomy.
153
FAECAL STOMAS
These may be temporary, loop or end type as
shown in Fig. 10.4; their appearances are
different, as are the difficulties in their management.
Small bowel effluent from an ileostomy will
irritate the skin and so the stoma is formed as
a spout, whereas a colostomy will be flush to
the skin since the effluent is more solid and less
irritant. If a bridge is used for a loop stoma, the
operation notes should be very clear as to how
long it should remain.
Irrespective of type, if there is concern with
respect to the stomas condition or function it
should be inspected, which will require:
Removal of the stoma bag
Assessment of the colour/perfusion of the
stoma and the contents of the bag (is the stoma
actually functioning? Is there any blood to
indicate more proximal bleeding?)
Assessment of the skin around the stoma
(is there cellulitis or separation of the stoma
from the skin? Is the stoma in close proximity
to wound giving risk of contamination?)
Digital examination of the stoma (and the
requirement for direct observation with a
proctoscope to determine the extent of any
discolouration).
Remember that while a complication of the
stoma may lead to systemic deterioration,
conversely systemic deterioration can lead to
stoma deterioration.
The small bowel effluent from an ileostomy is
usually 500700 ml/day but, initially, on starting
to function these volumes may be much greater
requiring careful electrolyte monitoring and
replacement.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
It is important to involve a stoma therapist as
early as possible, especially with respect to skin
protection. The therapist also provides vital
psychological support to the patients with a
stoma and, if possible, this meeting should
occur pre-operatively with marking of potential
stoma sites.
MANAGEMENT OF SURGICAL DRAINS
There is a continued debate as to the value and
usage of drains; nevertheless, their presence in
the critically ill surgical patient requires them to be
assessed and managed effectively and appropriately.
Within the assessment of the surgical patient, the
amount and type of drainage, and whether that is
expected, should be determined and documented.
The drain site should be inspected and notes
reviewed to determine the nature and positioning
of drains, and the rationale for placement. Drains
should be clearly marked if there is more that one
and it is the surgeons responsibility to state when
they should be removed.
POST-SURGICAL WOUND MANAGEMENT
Surgical wound infections are a common hospital
acquired infection (~12%) and are subsequently
an important cause of morbidity and mortality.
Therefore, their prevention should be a primary
management objective. The risk of infection
should relate to whether the surgery was clean,
clean with risk of contamination or contaminated.
It should not be a marker of hospital staff
hygiene! Remember to ensure good hand-washing
before and after the assessment of wounds to
diminish the risk of direct contamination.
A wound can be contaminated with bacteria
without a host response and then deemed to be
colonised when the bacteria multiply and initiate
154
a host response. When this bacterial multiplication
causes a delay in wound healing, the colonisation
is critical and is usually associated with wound
pain. Once there is both a delay in healing and
an associated host response the wound is infected.
By using the CCrISP method of assessment, all
wounds should have a postoperative plan with
observation for the early signs of infection of
redness, swelling, heat and pain. Dependent on
peri-operative risk and/or the potential consequences
of infection, the patient may have had prophylactic
antibiotics and this and any postoperative regimen
should be clear from a review of the charts. The
majority of wounds are closed primarily; however,
if there is local wound deterioration, it may be that
the sutures should be removed to allow drainage
or antibiotic treatment may suffice. The timings
of suture removal are a surgical decision and,
especially on ICU, should be clearly documented
within any surgical management plan.
SUMMARY
While it is sometimes difficult to assess the
post-surgical patient, particularly on the ICU, the
CCrISP process allows a structured assessment that
will highlight the likely cause of any deterioration.
By assessing the risk factors, many surgical-site
complications can be anticipated or recognised
early. Thus, postoperative management plans
should highlight which signs require early surgical
review, such as the increasing abdominal pressure
that would trigger the conversion to a laparostomy.
There will always be surgical complications
but the risk should be minimised and problems
should be recognised and managed promptly
and effectively.
11
Fluid and
electrolyte
management

155
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
be better able to manage complex fluid
balance in critically ill patients
be aware of common pitfalls in fluid
management in surgical patients
understand better water and electrolyte
balance in the critically ill
be aware of common electrolyte abnormalities
and their causes and management
understand the properties of common
intravenous fluids.
Assessing fluid balance and prescribing appropriate
fluid is an important daily task for surgeons; as
the registrar, it will be often be your responsibility
to ensure that this is carried out safely and
accurately. In many surgical patients, the process
becomes potentially complex because of multiple
sources of fluid loss and several types of fluid
input. However, with a logical approach and a
clear understanding of a few basics, even complex
cases can be dealt with. Conversely, poor prescribing
remains a common cause of avoidable morbidity
and mortality, either from inadequate resuscitation
of the critically ill or excessive provision of fluids
to elective patients.
156
PATIENT GROUPS
Patients are all different. Fluid needs are
determined by baseline needs (dependent, in turn,
on BMI), pre-existing fluid deficits and on going
abnormal losses. However, in major surgical
practice, we see two differing groups of patients
who handle fluids differently. Obviously, patients
may switch between groups if complications
develop.
CRITICAL ILLNESS
AND EMERGENCY SURGERY
In critical illness and after complicated major
surgery, the obligatory extracellular volume
required to maintain adequate venous return to
the heart rises due to the loss of salt water and
protein into sites of tissue damage, obstructed
bowel, serous body cavities and the relaxation
of the peripheral vascular bed. In some situations
(e.g. sepsis), the amount of sequestered fluid
may be prodigious due to an enormous capillary
leak and sufficient to cause circulatory failure.
This is the situation seen often in critically ill
surgical patients. Consequently, it is reasonable
to suspect hypovolaemia in most patients and
act accordingly.
Epidural anaesthesia causes vasodilatation and
this increased vascular space needs filling or
controlling. This is particularly so if the patient
has also been cold after surgery and vasodilates
further as they warm up. In these patients, the
commonest error is inadequate fluid resuscitation,
whether in volume, fluid type or rate of delivery.

UNCOMPLICATED ELECTIVE SURGERY
By way of contrast, major but uncomplicated
surgery produces a different situation. Surgery
itself causes activation of the anti-diuretic
hormone (ADH) and angiotensin-aldosterone,
thereby retaining fluids and causing reduced urine
output for 2448 hours. Thus, in a well patient
with otherwise normal parameters, isolated, modest
oliguria can be acceptable. With fast-track recovery
programmes advocating early and liberal oral
intake and less in the way of bowel preparation
(which dehydrates the patient significantly), the
elective patient is less likely to be volume
depleted. These patients often need much less
in the way of postoperative fluids; in these well
patients, excessive fluids cause more harm than
good. Here, excessive provision of sodium and
water is now recognised as the principal cause
of avoidable problems. This is a very different set
of circumstances to the critically ill patient who,
not infrequently, needs intravenous fluids rapidly
for life-saving resuscitation. Fluid resuscitation
from shock using an appropriate colloid or
crystalloid was dealt with in the chapters on
assessment and shock (Chapters 2 and 8).
CLINICAL ASSESSMENT
The patient should be fully assessed according to
the CCrISP system. Take particular note of indices
of volume status and perfusion, including vital
signs, CVP/JVP, skin perfusion and turgor and
oedema (which appears on the sacrum if bed-bound).
Note the patients underlying age, BMI, general
condition, operative treatment and timing,
co-morbid diseases and drugs.
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CHAPTER 11 | FLUID AND ELECTROLYTE MANAGEMENT
Along with clinical examination, the fluid balance
chart is the principal mechanism of assessment;
however, accuracy of fluid balance charts is variable
and, with experience, one learns which wards
charts can be relied upon the most! Insensible loss
increases markedly with fever, respiratory rate and
the breathing of dry O2 all of which can apply
in the day or two after major surgery. As much as
5001000 ml can be lost daily.
There is no one formula that can be applied to all
situations and regular frequent clinical assessment
of the patient will be required to adjust the content
and volumes of fluid replacement. This should be
done at least daily, more often in the unstable.
Occasionally with chronic overload, daily weighing
of the patient, when feasible, can be of assistance
and complements the fluid balance chart.
FLUID COMPARTMENTS
AND CONTROL OF VOLUME
The total body water volume (~45 l) is distributed
through the intracellular and extravascular
compartments in a ratio of 2:1 (Fig. 11.1).
The total volume of water is controlled by both
central osmoreceptors and volume receptors
that affect thirst and the release of ADH. Volume
receptors will release ADH even in the face of
hyponatraemia and a low plasma osmolality.
Extracellular fluid (ECF) volume (of which blood
volume is a special part) is maintained by the
presence of sodium and its accompanying anions
which are largely excluded from the intracellular
compartment by the action of the Na/K pump.
The body responds rapidly to a fall in central
volume or renal perfusion by reducing renal sodium
excretion to extremely low levels. Thus, there are
two mechanisms for retaining water or sodium
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Body weight
70kg

Total body water Fat, protein and mineral

60% = 42l 40% | 28kg

Intracellular Extracellular
66% = 28l 33% = 14l

Interstitial fluid Plasma

11l 3l

Figure 11.1 Fluid distribution in the body.

rapidly. On the other hand, excretion is more
passive and often slower, so the response to
surgical stress favours fluid retention and overload.
In critical illness this has some advantages, as
many of the effects of surgery cause fluid loss.
When assessing patients, consider:
assessment of fluid and electrolyte status requires
both clinical and biochemical examination
intracellular volume is extremely difficult
to assess clinically
the extracellular compartment is easier to
assess clinically as increased salt and water
manifests itself as oedema and salt and water
depletion by effects on the circulation
the balance between blood volume and ECF
is maintained by the oncotic pressure and the
relative leakiness of the capillaries
in haemorrhage, the plasma volume is partly
replenished from the ECF
in sepsis, gross capillary leak and a low
oncotic pressure contribute to oedema and
hypovolaemia.
BIOCHEMICAL ASSESSMENT
This clinical re-assessment is assisted by
biochemical measurement, primarily of blood but
also, on occasion, of urine and other fluid being
lost from the body (e.g. fistula fluid).
WATER
Patients usually need 15002000 ml water daily,
depending on weight and fluid status. The basal
water requirement is 30-40ml/kg/day.

158
 CHAPTER 11 | FLUID AND ELECTROLYTE MANAGEMENT

SODIUM upon the relative quantity of water in the extra-

Normal basal requirements for sodium are 50100
mmol/day but this can vary a lot with surgical
illness. Drug solutions can contain significant
amounts of sodium. Care must also be taken to
ensure that a false value for sodium is not obtained
by venepuncture from a limb with a running
fluid infusion or if there is frank lipaemia (e.g.
intralipid administration).
Hyponatraemia
Often, the serum sodium gives a clearer idea of
the relative water state of the body than of sodium
status, hence clinical assessment is essential.
A patient with hyponatraemia of, for example, 125
mmol/l may be sodium depleted (hypovolaemic),
sodium replete or sodium overloaded (oedematous
due to cardiac, renal or hepatic disease) depending
cellular space (Table 11.1). Dilutional hyponatraemia
from excessive infusion of water (as 5% dextrose)
is still seen on surgical wards.
The management of hyponatraemia may be
rapid sodium chloride infusion, water restriction
or diuretic plus water restriction depending upon
clinical assessment of volume status. Remember
that water cannot be excreted by the kidney in
the presence of extracellular fluid depletion
(see above primacy of volume) and that the
syndrome of inappropriate ADH secretion can
only be diagnosed once the patient has been
shown to be in sodium balance.
Correction of hyponatraemia should be achieved
at a similar rate to that at which it developed to
avoid cerebral fluid shifts. Given normal renal

TABLE 11.1

HYPONATRAEMIA TYPES AND CAUSES

ECF volume ECF volume ECF volume

Low Normal/slightly raised High
(NaCl , H2O ) (NaCl normal, H2O +) (NaCl +, H2O +++)
Urine Na high Diuretics (excessive) Glucocorticoid deficiency Renal failure
(> 20 mmol/l) Salt losing renal disease Hypothyroidism
Mineralocorticoid SIADH
deficiency
Urine Na low Extrarenal loss: Dilutional
(< 20 mmol/l) (i) Outwith body (i.v. 5% dextrose)
(ii) Sequestration Cirrhosis
Cardiac failure
Nephrotic syndrome

159
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
function, water overload can be cleared by the
administration of diuretic and 0.9% sodium
chloride to replace the fluid excreted by the kidney.
Hypertonic saline is seldom necessary.
Hypernatraemia
This can be caused by abnormal intake or
administration of hypertonic fluid (e.g. 8.4%
sodium bicarbonate), but is more commonly due
to abnormal water loss (fever, diabetes insipidus
or mellitus, osmotic diuretics) in a situation where
intake of water is impaired. Correction is with
water (via the gut) or by intravenous 5% dextrose.
POTASSIUM
The usual requirement of potassium is 4080
mmol/day.
Hypokalaemia
Common causes of hypokalaemia in surgical
practice include: (i) renal losses; (ii) intestinal
losses; and (iii) medical losses (no K in the drip!).
Plasma potassium is a poor reflection of the total
body potassium content as plasma contains only
1% of the body total. The rate of change of the
extracellular potassium concentration is more
important than the absolute value. Hypokalaemia
is usually the result of loss of potassium from the
body via the kidney or bowel (diuretics, tubular
disease, diarrhoea or laxatives). Acute changes in
plasma potassium may occur as potassium moves
into cells during the correction of an acidosis,
secondary to the acute release of catecholamines
(cerebral bleed or trauma), administration of
salbutamol or upon refeeding with the start of
anabolic activity. The level should be kept above
3.5 mmol/l by stopping any avoidable losses and
the administration of potassium.
160
Hyperkalaemia
A rapidly rising plasma potassium level is a
medical emergency and will result in respiratory
muscle weakness and cardiac arrest from which
it is extremely difficult to be resuscitated.
The primary route of potassium excretion is via
the kidney in the distal nephron under the influence
of aldosterone. Renal failure, hypoadrenalism,
distal nephron disease (e.g. chronic obstructive
nephropathy) or drugs that affect the renin
aldosterone system (e.g. ACE inhibitors) will all
impair the excretion of potassium. Where there
is a sudden movement of potassium out of cells
due to trauma, drugs (suxamethonium), ischaemic/
hypoxic damage or a sudden rise in hydrogen
ion concentration, patients with impaired renal
excretion will be particularly vulnerable.
A classical example is the hypovolaemic patient
with a metabolic acidosis plus respiratory
compensation who has anaesthesia induced with
suxamethonium, is then underventilated with
consequent sudden fall in pH and suffers a
cardiac arrest shortly after induction. There is
no absolute level above which the signs and
symptoms appear and effects are related to the
rate of rise as much as the plasma concentration.
A chronic potassium level of 6.0 mmol/l will be
well tolerated but may be fatal if the result of
a rapid change from 4 mmol/l. Levels of this
magnitude require rapid, specific treatment (see
Chapter 9) plus reversal of the primary condition
and removal of any precipitant drugs, if possible.
CALCIUM
The calcium level in the plasma is normally kept
within a narrow range under the influence of
parathyroid hormone, 1,25-dihyroxy-vitamin D3
and renal function. The active component is the

ionised fraction which is unbound to albumin.
Total levels have to be regarded in relation to the
albumin level or the ionised fraction has to be
measured directly.
Hypercalcaemia
Severe hypercalcaemia will affect neural tissue
and damage renal tubular function. In the critically
ill, this is most often due to paraneoplastic
hypercalcaemia. Hypercalcaemia diminishes the
kidneys ability to retain salt and the resultant
hypovolaemia reduces the ability of the kidney
to excrete calcium. Dysrhythmias may occur.
Establishing a saline diuresis will normally help
reduce the level. If this fails, the administration
of a bisphosphonate intravenously will reduce
the level of calcium. Effective treatment of the
primary cause will also bring the level back to
normal. The development of hypercalcaemia in
association with recurrence of a solid tumour
is usually an indication of a poor prognosis.
Hypocalcaemia
Apparent severe hypocalcaemia may be found in
the critically ill if total plasma level is measured
without reference to the albumin level. An
absolute hypocalcaemia level is seen in acute
pancreatitis, acute rhabdomyolysis and following
thyroid surgery. Treatment is by the administration
of calcium, treatment of the primary condition
and in post parathyroidectomy syndrome or
vitamin D deficiency, administration of activated
vitamin D analogues. In those situations of critical
illness with intact parathyroid function, aggressive
administration of calcium should be limited to
situations where there is clinical evidence of
hypocalcaemia rather than attempting to achieve
a given value.
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CHAPTER 11 | FLUID AND ELECTROLYTE MANAGEMENT
MAGNESIUM
Magnesium is the second most important
intracellular cation after potassium. Magnesium
is essential for the normal functioning of nerve
and muscle. Depletion causes confusion and
seizures and is associated with a range of
dysrhythmias, while excess causes muscle paralysis
and central nervous depression. In the critically
ill, hypomagnesaemia is common in the early
recovery period of severe insults such as peritonitis.
Chronic losses from the bowel (diarrhoea), kidney
(loop diuretics), and alcohol abuse contribute. As
with potassium, plasma levels reflect total body
magnesium poorly but a plasma level below 0.6
mmol/l associated with a condition likely to cause
magnesium deficiency or the presence of symptoms
should precipitate supplementation. This is best
done intravenously in the acute stage to avoid the
purgative effects of magnesium salts. The plasma
level should not exceed 1.5 mmol/l. Critically ill
patients with dysrhythmias should have magnesium
levels checked as treatment with magnesium
contributes to the control of several dysrhythmic
states.
Significant hypermagnesaemia is almost always
secondary to iatrogenic administration in the
presence of impaired renal function (e.g. as
magnesium sulphate for eclampsia).
PHOSPHATE
Phosphate is present in any protein containing
food and is absorbed from the gut. The kidney
excretes phosphate under the influence of
parathyroid hormone. High levels will be seen
in renal impairment or following massive muscle
or bowel necrosis. In the short term, this is usually
not a major problem unless large quantities of
calcium are administered.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Hypophosphataemia is commonly seen during
recovery from critically illness: as cell function is
restored, phosphate is taken back into cells with
potassium and magnesium. When the phosphate
level falls below 0.6 mmol/l, there are effects that
can be measured regarding respiratory and other
skeletal muscle function plus effects upon the
functioning of the immune system. Replacement
will come with feeding but, with levels below 0.6
mmol/l, intravenous supplementation will be
required given slowly over 24 hours.
TRACE METALS
There are many trace metals that are essential to
normal cellular function and the healing process
(e.g. zinc, copper and selenium). In situations
where there is prolonged dependence upon
parenteral feeding or prolonged gut dysfunction,
consideration must be given to the measurement
and necessary supplementation of their intake.
APPROACH TO THE PRESCRIPTION
OF FLUID AND ELECTROLYTES
This should be read in conjunction with the
section in the chapter on nutrition (Chapter 13).
In the critically ill, fluid replacement will be guided
by the clinical situation, which is constantly
changing. Requirements will be dependent upon
many factors, but with three main headings: (i)
basal requirements; (ii) existing fluid and electrolyte
excess or deficit; and (iii) continuing abnormal
losses.
162
Basal requirements (15002500 ml of water,
100 mmol Na and 80 mmol K) are influenced
by a number of factors including body weight
(Table 11.2). Age and cardiac or renal disease
can jeopardise the patients ability to correct
imbalances so greater care is then needed.
Intravenous fluids should be used for as short
a period as possible this is particularly so in
well patients (e.g. after elective surgery).
Pre-existing fluid and electrolyte excess or deficit
need factoring in potassium deficit takes some
time to correct, for example. Oedema takes some
days to resolve, typically as the surgical patient
recovers from major surgery and the epidural is
removed.
Abnormal losses usually change gradually. These
might include insensible loss of water dependent
upon fever, continuing loss from the gastrointestinal
or renal tract, or other effects of recent surgery,
with fluid redistribution or loss from open
wounds. As well as noting yesterdays outputs,
your clinical assessment should help you predict,
to some degree, how these losses might change
today. For example, a patient recovering from
laparotomy with a soft abdomen and now passing
flatus, may be expected to tolerate more oral
intake successfully. Hence previous nasogastric
losses will likely resolve and need for intravenous
fluid will decrease as oral intake increases.
On the other hand, we need to be realistic
about tolerance of oral intake in ill patients.
Just because it is prescribed or permitted, does
not mean it will be taken or tolerated. If, at this
point, the fluid balance is no longer charted,
then problems may develop.

TABLE 11.2
SOME CONSIDERATIONS
FOR FLUID THERAPY
Fluid isotonic for sodium will be required
to maintain adequate extracellular volume.
Water (oral or 5% dextrose) is needed to
maintain intracellular volume and provide
sufficient volume to excrete the renal load
of solute waste.
The volume of clear intravenous fluids
will need to be reduced depending on the
volume being given by other routes or forms
(drugs, oral intake, nutrition, blood, etc.).
Electrolyte deficiencies will need to be
corrected as well as basal needs being met.
REPLACING ABNORMAL LOSSES
As a general rule, abnormal losses should be
replaced with a fluid having the same composition
as that which is being lost, and in a similar volume.
However, matching the fluid exactly is not always
necessary as the kidneys compensate efficiently
under many circumstances.
Losses can be divided into those that consist more
or less of extracellular fluid (ECF) or its equivalent,
and those that are mainly or purely water (Table
11.3). Clearly, some conditions have elements
of both.
When there is loss of an ECF-equivalent fluid,
there is a decrease in the total ECF volume and
this includes the plasma volume.
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CHAPTER 11 | FLUID AND ELECTROLYTE MANAGEMENT
TABLE 11.3
FLUID LOSSES
Losses that approximate extracellular fluid
Blood loss
Vomiting
Diarrhoea
Gut fistulae
Postoperative third space sequestration
Systemic inflammatory response syndrome
(e.g. sepsis, burns, pancreatitis)
Diabetes mellitus (hyperglycaemia)
Losses that are principally water
Fever
Increased respiratory rate
Prolonged water deprivation
Diabetes insipidus
This deficit should be replaced promptly to restore
perfusion to cells and vital organs. Abnormal
losses of water with or without electrolytes
(particularly sodium and potassium) will result
not only a reduction in plasma volume but
also a marked change in intracellular fluid volume
and the concentrations of important ions across
cell membranes. Restoration of the plasma
volume always takes precedence, and should be
accomplished with a balanced salt solution
(see below).
Restoration of the water deficit and other
electrolyte deficits can then be addressed. This
should be accomplished gradually so that rapid
shifts of water across membranes, especially the
blood/brain barrier, are avoided. It takes much
longer for electrolytes to equilibrate between
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
some compartments, and the resulting osmotic
gradient can lead to fatal cerebral oedema or
other complications if therapy is too hasty.
Aim to correct these over 4872 hours.
REPLACING EXTRACELLULAR FLUID LOSS
Central to the replacement of ECF deficits (blood
volume, interstitial volume) is the use of a balanced
salt solution. This term refers to a crystalloid
solution which is isotonic (and remains so) and
has constituents that are similar to the ECF,
(normal saline or 0.9% sodium chloride, lactated
Ringers buffer also known as Hartmanns
solution). When a balanced salt solution is given,
it will distribute itself throughout the extracellular
compartment (~14 l) over several minutes.
Only about a third of the volume given will
remain in the vascular space. Understanding this
phenomenon will prevent undertreatment of blood
volume deficits when using balanced salt solutions.
As reduced intravascular volume is usually
accompanied by an ECF deficit, redistribution of
balanced salt solution into the interstitial space
is usually desirable. Normal saline contains too
much chloride for physiological needs and, with
over-prescription, hyperchloraemia (and acidosis)
occur. Hartmanns solution does not cause this.
In a situation where the volumes required are
large, maintenance water and electrolytes are
often forgotten. This seldom matters in the first
24 hours or so because the volume shifts are so
large and the kidney can usually sort out what it
wants to keep or excrete. However, as time goes
on, maintenance water needs to be thought about
or the patient will become hypernatraemic and
hyperosmolar.
164
VOMITING, DIARRHOEA AND
INTESTINAL FISTULA LOSSES
These gastrointestinal conditions cause losses
of fluid which resemble ECF although typically of
a lower osmolality (i.e. more water is lost relative
to sodium). The result is blood volume depletion,
dehydration, and large electrolyte losses. If water
only has been taken orally to try to compensate,
hyponatraemia may be present; however, if serum
sodium is normal or even high, the possibility of
a significant sodium deficit must not be overlooked.
In some conditions (e.g. vomiting from complete
upper small bowel obstruction, diarrhoea due to
cholera) the volumes lost can be huge and rapidly
life-threatening.
Potassium depletion is universal, and may be
severe with marked diarrhoea. Metabolic acidosis
may mask the extent of total body potassium
deficit by causing potassium to move from within
cells to the extracellular compartment in exchange
for extracellular hydrogen ions.
Additionally, vomiting or nasogastric drainage
leads to loss of hydrogen (H+) and chloride (Cl-)
ions from the stomach. This can produce a marked
metabolic alkalosis but, despite this, it is rare that
H+ needs to be given intravenously. Adequate
chloride replacement in the form of normal saline
will usually correct the deficit, as endogenously
produced acid (H+) will be retained by the kidney.
By using fluid balance charts and clinical
assessment logically to keep total volume and
key ions, particularly sodium and potassium,
in balance, you can achieve success in the great
majority of cases. However, there is no single
formula for success and patients change
continually so re-assess!
 CHAPTER 11 | FLUID AND ELECTROLYTE MANAGEMENT

CASE SCENARIO 11.1

A 58-year-old, 70kg man, otherwise fit except for long-standing AF controlled with digoxin,
underwent a cystectomy for bladder cancer 3 days ago. An ileal urostomy was constructed,
necessitating a small bowel anastomosis. Presently, he is on HDU, is apyrexial and his chest is
clear (respiratory rate 16/min), but his abdomen is rather distended. Although his urine output is
rather low, he seems reasonably well perfused. The monitor shows AF at a rate of 118 bpm. It is
Saturday and you are on-call the HDU nurse has asked you to sort out his fluid balance for the
weekend. Review the fluid balance chart below and prescribe his intravenous fluid. His consultant
wished him to stop antibiotics after 72 h.
WHAT FURTHER INFORMATION DO YOU REQUIRE?
WHAT WOULD YOU PRESCRIBE AND HOW?
ARE BLOOD TESTS NECESSARY TODAY?
WHEN SHOULD YOU REVIEW FURTHER?

DATA

Intake summary CVP line Peripheral line (R) Peripheral line (L) Oral

(last 24 h) Normal saline Dextrose 5% Antibiotics (600 ml), Sips

(975 ml) (1800 ml) PCA (125 ml) (120 ml)

Losses summary Nasogastric tube Pelvic drain Urostomy Bowels

(last 24 h) 1450 ml 720 ml 640 ml Nil, no flatus

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CASE SCENARIO 11.1 ANSWERS

This is clearly a complex case who is not yet clinically stable. In addition to making your own
clinical assessment, you should review the fluid charts from the previous day or two to look for
patterns and for accumulating losses or excesses. Look at the operation note for any specific
postoperative orders. Urinary anastomoses may leak for a few days so urine appears through
the drain as well as the catheter and/or urostomy. Ileus can be prolonged and nutritional support
may be needed but, again, this is not pressing at 72 h postoperatively. You clearly need to review
yesterdays biochemistry results (Na 138, K 3.1, urea 5.2) and repeat these today. Summate the
data above and include insensible loss about 750 ml is probably reasonable here, but revise the
factors which influence this.
His needs are probably about 3500 ml the water requirement (5% dextrose 2000 ml) will be
unchanged the excess volume should be crystalloid (1500 ml). His antibiotics will be stopped,
but his PCA will continue. You will need to give at least some of the fluid via the CVP line to keep
it open. He is hypokalaemic and you should aim to give 80 mmol K over the next 24 h you may
modify this when you review with the blood results later. This need is the more pressing because
of his AF and digoxin therapy. If K replacement and digoxin fail to control the rate then the
magnesium level should be ascertained.
It is obviously inappropriate to prescribe for the whole weekend just now. Some losses the
nasogastric loss for example may increase or decrease and clinical and biochemical re-assessment
is needed. Plan to review with your team at the end of today and again at 8 a.m. tomorrow.

SUMMARY aim to correct electrolyte values may be

fluid and electrolyte imbalance is common active or passive
and detrimental use urine electrolytes, weight and plasma
accurate fluid balance is achievable with osmolality when needed.
a logical approach
consider basal requirements based on patient FURTHER READING
size and age Powell-Tuck J, Gosling P, Lobo DN et al.
consider abnormal on going losses, pre-existing British Consensus Guidelines on Intravenous Fluid
deficits or excesses, fluid shifts Therapy for Adult Surgical Patients (GIFTASUP).
normal renal and cardiovascular function London: NHS National Library of Health, 2008.
protect against fluid intolerance
look at the fluid balance chart for last 24 hours.
Are all fluids given or lost included? Do the
volumes seem right from other available
information? Check previous charts for
insidious changes

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12
Sepsis and
multiple
organ failure

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the definitions associated
with systemic inflammation and sepsis
understand the clinical pathophysiology
of the septic process
appreciate that prevention, early diagnosis
and prompt treatment of sepsis are many
times more successful than treatment of
established septic shock
understand the essential features of the
Surviving Sepsis Campaign
understand a system for the management
of the septic patient
understand the roles of antibiotics, surgery
and other interventions in the management
of sepsis.
The number of patients at risk of major sepsis
progressively increases each year. Patients with
indwelling catheters, those in ICU or HDUs, those
being treated with chemotherapy or steroids, are
individuals at particular risk. In addition, the
ageing population and the ability to treat patients
with major chronic illness increases the complexity
of management of patients with sepsis. In the US
at present, septic shock is estimated to account for
about 100,000 deaths annually and the mortality
has changed little in the past 30 years; the
mortality of surgical patients with major sepsis/
septic shock continues at the level of about 50%.
It is important to recognise that the signs and
symptoms associated with sepsis are caused by
the release of endogenous mediators. This mediator
release may be precipitated by a variety if
168
insults, including infection and trauma
(Fig. 1). The mediators involved include nitric
oxide, bradykinin, histamine, prostaglandins
and cytokines, all of which have vaso-active
properties. They produce a state of vasodilatation,
enhanced capillary leak and eventually
myocardial depression.
Other
Bacteraemia
Trauma
Infection
Severe Sepsis SIRS
Fungi
Burns
Parasites
Other
Pancreatitis
Figure 12.1 Interacting factors that result in sepsis.
Cytokines involved include interleukin-1
(endogenous pyrogen), tumour necrosis factor
and interleukin-6. Released from the patients
own white blood cells, these contribute to the
patients pyrexia and hypermetabolic state.
While production of mediators is needed to
combat infection, an excessive or prolonged
activation of such cellular and humoral mediator
pathways is thought to contribute to the
development of multiple organ failure (MOF)
in patients with major sepsis.
A balance exists between inadequate and
excessive responses to infection. Inter-individual
variation in the pattern of mediator release and
of end-organ responsiveness plays a significant
role in determining the initial physiological
response to major sepsis and this may be a
 CHAPTER 12 | SEPSIS AND MULTIPLE ORGAN FAILURE

determinant of outcome. Other important prognostic
features include the severity of the initial trigger
event, the timeliness and adequacy of treatment
of the underlying condition and the patients
general state of health.
DEFINITIONS
The systemic inflammatory response syndrome
(SIRS) and sepsis is a spectrum of illness ranging
from mild systemic disturbance (typically seen in
the early postoperative patient) to life-threatening
multiple organ failure. A consensus conference
(Barcelona, 2001) agreed the now accepted
definitions outlined in Table 12.1. All involve
a systemic derangement which distinguishes them
from localised infection.
As described above, many surgical patients
have evidence of SIRS, and the vast majority

TABLE 12.1

CONSENSUS CONFERENCE DEFINITIONS IN SEPSIS

Systemic inflammatory response syndrome

(SIRS, also known as symptoms and signs of infection or SSI)
Two or more of:
pyrexia (> 38C) or hypothermia (< 36C)
tachycardia (> 90 bpm in absence of -blocker)
tachypnoea (> 20 breaths per minute or a requirement for mechanical ventilation)
white cell count > 12 or < 4
acutely altered mental state
blood glucose of > 6.6 in the absence of diabetes
Sepsis = SIRS + documented source of infection
Severe sepsis (confirmed infection) or sepsis syndrome (no confirmed infection)
SIRS + altered organ perfusion or evidence of dysfunction of one or more organs. Almost any
organ or system can be involved, including:
CVS (lactate > 1.2 mmol/1 or SVR < 800 dyne/s/cm3)
respiratory (PaO2/FiO2 < 30 or PaO2 < 9.3 kPa)
renal (urine output < 120 ml over 4 h)
CNS (GCS < 15 in absence of sedation/neurological lesion).
It is important to note that the identification of organ dysfunction is initially a clinical diagnosis.
You should think about organ dysfunction/failure in any critically ill surgical patient who looks
breathless, has poor perfusion, confusion, poor urine output or abnormal coagulation.
Septic shock
Refractory hypotension in addition to the above, in the presence of invasive infection

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will recover uneventfully with good surgical care.
However, the presence of such signs, particularly
when persistent, serves as a warning of the
potential for deterioration in the absence of
prompt treatment. SIRS may result from an
infective process or other conditions, including
pancreatitis, ischaemia, multiple trauma or
haemorrhagic shock.
When such a response is due to an identified
infective process, it is known as sepsis; when it is
associated with organ dysfunction, hypoperfusion
or hypotension, it is termed severe sepsis
(infective cause) or sepsis syndrome (no identified
infection).
The septic picture can be caused by surgical and
non-surgical factors and, as indicated above, can
occur with confirmed infection or in its absence.
Although specific criteria for organ dysfunction
exist, you should be actively looking for clinical
evidence of organ derangement (e.g. dyspnoea,
hypoxia, oliguria, jaundice, thromobocytopenia)
in all susceptible patients.
The essential points of management of the patient
with sepsis include:
early recognition
immediate resuscitation
localisation of sepsis
early and appropriate administration of
antibiotics
appropriate management of the primary
source of sepsis including the use of surgical
or radiological drainage
on going re-assessment to ensure the patient
continues to improve.
Failure to accomplish any of these promptly will
markedly worsen the prognosis.
Table 12.2 shows some causes which you will
encounter. The classification might help you

TABLE 12.2

POTENTIAL CAUSES OF SIRS

Infective Non-infective
Non-surgical Pulmonary Acute pancreatitis
Urinary and catheter-related Re-perfusion injury
Intravenous lines, especially CVP
Soft tissue infection
Surgical Anastomotic leak Ischaemic gut
Biliary especially if obstructed Ruptured aorta
Urinary with obstruction Major haemorrhage
Collection/abscess Trauma
Infected prosthesis (hip, aortic graft,
heart valve, neurosurgical shunt)
Necrotic tissue

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remember them but a number of the causes could
appear in different boxes depending on the stage
(e.g. ischaemic gut). Surgical ones often require a
surgical solution but all causes occur in surgical
patients.
PATIENT ASSESSMENT
AND MANAGEMENT
IMMEDIATE CARE
Remember the ABCs: patients with major sepsis
may have a tachypnoea and have cardiovascular
changes. The presence of these changes demands
high-flow oxygen via a facemask and establishment
of intravenous access with volume expansion by
appropriate fluid bolus at a minimum.
FULL PATIENT ASSESSMENT
Chart review
Vital signs should be reviewed carefully:
tachypnoea, tachycardia, hypo- or hyperthermia
are all consistent with sepsis. A CVP between
510 cmH2O and a urine output greater than 30
ml/h are reasonable guides to the adequacy of
initial fluid resuscitation. If hypotension/inadequate
perfusion persists despite adequate fluid replacement
and CVP monitoring, then inotropic support
should be considered, which will require input
from colleagues experienced in critical care and
involve additional monitoring.
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CHAPTER 12 | SEPSIS AND MULTIPLE ORGAN FAILURE
History and systematic examination
An assessment of the patients presenting complaint
may help to establish the likely source of sepsis:
breathlessness and a productive cough may
indicate a pulmonary source
abdominal pain or bowel symptoms may point
to an abdominal problem. An abdominal or
pelvic abscess may cause diarrhoea or an ileus:
anastomotic leaks are common and can be subtle
frequency, dysuria or haematuria are common
in urinary sepsis, which can often implicate
the urinary tract. Beware the combination of
obstruction with infection (usually due to a
stone), as sepsis may be severe and permanent
renal damage can occur rapidly
headache and neck stiffness may point to
a source in the central nervous system.
Remember, however, that confusion is common
in the unwell septic patient and does not
necessarily indicate a source in the CNS.
The systemic review should also evaluate chronic
health problems and current medication which may
suggest a susceptibility to sepsis (e.g. use of steroids)
or may indicate the need for more intensive
monitoring (e.g. recent myocardial infarction).
The history and examination may be very useful
in helping to indicate the source of the problem.
Common things occur frequently: chest infection,
anastomotic leak, central line infection are
often implicated in the recovering surgical patient.
Timing of events can also help: the chest is a
common early cause of postoperative fever or
sepsis from day 1 onwards while anastomotic leak,
as mentioned previously, usually occurs from day
4 and central line infection becomes more frequent
in lines more than 48 hours old.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 12.1

As the surgical trainee on the HDU 8 a.m. ward round, you review a 73-year-old woman with mild
COAD who had a left hemicolectomy with primary anastomosis for colonic carcinoma 6 days ago.
You are told that the white blood cell count was 16.3 yesterday, increased from 8.5 the day before.
WHAT WOULD YOU DO?
Systematic assessment shows that her ABCs are stable. The charts show an increased heart rate
(was 70 bpm, now 95 bpm), a temporary pyrexia of 38C over night and decreased urine output
(only 25 ml/h for the last 3 h). The patient has no specific complaints but has been generally slow
to recover. The CVP line is still in situ, as is the epidural and the urinary catheter. Examination of
her chest is unchanged, and shows a few basal crackles, but stable gas exchange and she is able to
expectorate adequately without pain. Her abdomen is slightly distended, and flatus has been passed
but no faeces. There is no evidence of a DVT. Macroscopically and on dipstick, her urine is clear.
WHAT WOULD YOU DO NOW?
Now is the time to decide and plan! The patient is not quite right but has no definite signs.
There are a number of potential sources of sepsis (chest, CVP line, urine, urinary catheter, abdomen,
anastomosis). Peripheral blood cultures and cultures through the central venous line should be sent,
as should urine and sputum cultures. A chest X-ray should be ordered if there is not a recent one,
a fluid challenge started and the physiotherapist called.
When reviewing such a case, the operation performed (which includes a primary colonic anastomosis),
the stage of recovery and the fact that her gut has still not started working again should make you
consider an anastomotic leak. You discuss the case with your consultant and arrange a contrast-
enhanced CT scan. A small, localised leak is suspected. Your consultant thinks that the patient may
settle, and takes a conservative approach to further management. Antibiotics are prescribed and the
patient is fasted.
ON REVIEW
Overall, the patient appears to remain unchanged throughout the next 24 h. There is one further
flicker of pyrexia (37.8C). The heart rate remains at 95100 bpm. The next morning, her abdomen
is still distended and her ileus persists. The urea has climbed to 10.4 and patient had a run of fast
AF at 5 a.m. despite a CVP of +9 and normal saturations. 12-lead ECG and cardiac enzymes were
normal but Mg level was low. This has been corrected.
Your consultant joins you and together you decide that the failure to respond (abdomen, heart rate)
and the recent cardiac and renal effects are more than enough to require surgery to deal with the
leak. After appropriate resuscitation, she is taken to theatre where the anastomosis is taken down
and the ends exteriorised. The patient returns to HDU and makes an uncomplicated further recovery.

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LEARNING POINTS
The causes of postoperative pyrexia and of sepsis in surgical patients are not the same:
anastomotic leaks are not uncommon
they may present with a variety of features, often between day 4 and day 8
symptoms range from the catastrophic collapse into MOF to subtle derangements of vital
signs or biochemical parameters, or failure to progress
gut function is usually delayed or absent (but not always!)
surgical or radiological intervention is often required
organ dysfunction requires prompt action
the intervention required depends on the site and the previous operation but leaking small
bowel and colonic anastomoses are usually best exteriorised as stomas.

Available results Aerobic and anaerobic blood cultures are

Review available results and arrange new
investigations.
The white blood cell count may be abnormally
high (> 10 x 109/l) or low (< 2 x 109/l) in major
sepsis. A coagulation screen should be checked,
particularly if surgery is contemplated: thrombo-
cytopenia and coagulopathies are common and
should be corrected before surgery.
The urea and electrolytes should be reviewed with
particular attention to renal function: acute renal
failure is a frequent complication of severe sepsis
and is often preventable in the early stages by
adequate fluid resuscitation.
Liver function tests may be abnormal, particularly
when the biliary tree is the primary source of sepsis
or as part of a multi-organ failure syndrome (MOFS).
An ECG should be checked for evidence of
ischaemia or arrhythmia.
ABGs should be taken and may show hypoxaemia,
with or without a metabolic acidosis.
obligatory but will only be positive in about 20%
of cases. A higher positive culture rate can be
achieved if the primary source of sepsis can be
cultured (e.g. pus from an abscess, urine from an
infected system). Sputum, urine, drain fluid and
pus from wounds should be sent for culture and
sensitivity. Cultures should also be taken through
in-dwelling central venous catheters. Fungal
infection should be considered, particularly when
the diagnosis is proving elusive or there have
been multiple previous courses of antibiotics.
Empirical treatment with antibiotics can be started
on an educated guess basis (with advice from the
microbiologists locally). These can be changed
when results of culture and antibiotic sensitivity
become available.
Further evaluation of possible sites of sepsis
include the use of ultrasound, CT scanning and
laparotomy. Remember the adage, pus somewhere,
pus nowhere, pus under the diaphragm. Patients
who are immunocompromised (e.g. transplant
patients) may develop opportunistic infections

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which may require very specific investigation through attention to detail and gives the patient
(e.g. broncho-alveolar lavage or transbronchial the best chance of avoiding further deterioration.
biopsy for those with pneumonia). Features to consider include the following.

DAILY MANAGEMENT PLAN: Fluids

THE STABLE PATIENT
A daily management plan is needed for all patients,
no matter how stable they appear to be. This ensures
that all members of the multidisciplinary team know
what is going to happen. A list of clear, positive
decisions listed in the patient record provides a plan
for genuine progress. The aim is to ensure progress
It is important to hydrate all patients adequately
to allow good tissue perfusion. Crystalloids are
usually appropriate fluid replacement: colloids may
remain in the circulation longer but, when they
escape to the tissues, may worsen oedema. Patients
with sepsis syndrome may require up to 1012 l
of fluid in the first 24 hours of resuscitation.

CASE SCENARIO 12.2

A 61-year-old, previously fit, woman was admitted to the ward 4 days ago with acute sigmoid
diverticulitis. Initial signs included minimal tenderness in the left iliac fossa. Treatment was started
with a second generation cephalsosporin and metronidazole. Fever and leukocytosis settled within
48 h. She has suddenly become acutely unwell, with recurrent tenderness in the left iliac fossa,
pyrexia of 39.2C, tachycardia and hypotension.
WHAT WOULD YOU DO AT THIS STAGE? WHAT IS YOUR DIFFERENTIAL DIAGNOSIS?
It is clear that the patient has deteriorated markedly despite initial treatment for her presumed
diagnosis: a change of treatment is needed. Following resuscitation (including blood cultures and
biochemical tests) and after discussion with her consultant, an experienced surgical trainee takes
the patient to theatre for an emergency sigmoid colectomy. There is a 7 cm pelvic abscess beside
the inflamed sigmoid colon, which is drained and a sample of pus sent for urgent microbiological
examination and culture. A Hartmanns procedure (sigmoid colectomy with colostomy and
closure of the rectal stump) is carried out and the patient returned to HDU in stable condition.
Peri-operative antibiotics were given as previously and prescribed for a further 5 days.

LEARNING POINTS
anticipate from the initial diagnosis and your knowledge of common complications
resuscitate adequately monitor and get help as necessary
cultures blood and source
antibiotics best guess then selective and in short courses
definitive surgical treatment is essential.

174

Care should be taken to avoid fluid overload, and
such large volume fluid resuscitation is likely to
require guidance by using additional monitoring
(e.g. CVP or cardiac output monitoring).
Oxygen
It is essential that the patient does not become
hypoxaemic: oxygen should be administered
as required to correct hypoxaemia. If facemask
oxygen is inadequate, consideration should be
given to additional respiratory support, which
will usually require help from ICU colleagues.
Nutrition
It is essential to ensure adequate metabolic and
nutritional support of the patient in order to optimise
the patients endogenous immune function. This
can be by the enteral or parenteral route.
Antibiotics
Antibiotics must be given as early as possible.
Empirical treatment on a best-guess basis should
be started with microbiological advice. It is
important to review the microbiology after 48
hours when cultures are available and sensitivities
obtained: discussing cases with the microbiologist
can be very helpful and is to be recommended.
It has been shown clearly that the mortality of
patients is significantly lower when appropriate
antibiotics are prescribed early in the course of the
patients illness. It is also important to appreciate
that fungi and atypical organisms can contribute
to the sepsis syndrome and to take cultures and
prescribe appropriately. Prolonged prophylaxis
is not recommended, as super-infection by fungi
and antibiotic-resistant organisms is encouraged.
Finally, remember that enteric streptococci
account for 1020% of severe infections related
to the abdomen and that they are not sensitive to
all common prophylactic antibiotics.
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CHAPTER 12 | SEPSIS AND MULTIPLE ORGAN FAILURE
Additional considerations
Instructions for physiotherapy, DVT prophylaxis
and, in a patient with ongoing abdominal sepsis,
drain management should also be included in
the daily management plan.
DIAGNOSING CAUSE OF DETERIORATION:
THE UNSTABLE PATIENT
In a patient with new or ongoing sepsis,
deterioration may be elicited by pyrexia, clotting
disturbances, a metabolic acidosis and/or organ
dysfunction. Alternatively, the patient may simply
fail to progress. The presence of such a pattern
demands careful clinical review of symptoms and
signs, repeat microbiology, review of antibiotic
sensitivities and may require further radiological
evaluation with either percutaneous or operative
drainage of localised sepsis. Failure to diagnose
significant sepsis will prove fatal.
Definitive treatment
Definitive treatment is the single most important
factor in securing survival. Localised collections
of pus generally need either operative or
percutaneous drainage and dead tissue should
be excised.
Severe pulmonary sepsis requires adequate
antibiotics and chest physiotherapy. It may also
require repeat bronchoscopy and toilet of the
bronchial tree, and additional respiratory support
(NIV, IPPV).
In spreading soft tissue infection, it is important
to establish adequate drainage and vital to excise
necrotic or devitalised tissue as well as giving
antibiotics. Repeated examination under anaesthesia
with further debridement is usually needed.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Abdominal sepsis, if localised, may be treated
initially with antibiotics or percutaneous drainage,
but generally the primary source of sepsis must
be removed. Copious intra-operative peritoneal
lavage is important and you should be alert to the
development of recurrent sepsis during subsequent
assessments of the patient.
A planned, second-look laparotomy may be
useful, particularly in patients with equivocal
bowel perfusion during previous procedures.
Obstruction of the biliary or urinary system must
be relieved. An infected prosthesis will usually need
to be removed (e.g. peripheral or central venous
cannulae, urinary catheters, prosthetic metalwork).
Sometimes, such decisions are difficult and
will require discussion between different medical
teams. Vigilance around the possibility of
catheter-associated sepsis, particularly in patients
in the HDU or ICU, is essential.
MRSA infection is becoming more common in
all patients. It is important to distinguish between
patients who are colonised carriers and those
with MRSA sepsis. Whereas MRSA colonisation
does not present major problems in most patients,
it may do in those patients with prostheses (aortic
valves, aortic grafts, hip replacements) where it
is associated with a very high mortality. Often,
the only treatment is removal of the prosthesis
and long-term antibiotics. Microbiological help
is essential.
PREVENT DIAGNOSE ACT
THE SURVIVING SEPSIS CAMPAIGN
The Surviving Sepsis Campaign (SSC), a
collaborative initiative developed by 11
international societies, was launched in 2002.
The aim of the SSC is to reduce mortality from
severe sepsis. Initial guidelines were announced
in 2004, and updated in early 2008 to respond
to latest evidence.
The SSC includes two recommended management
packages or care bundles the Resuscitation
Care Bundle and the Management Care Bundle.
The SSC Resuscitation Care Bundle
The Resuscitation Care Bundle aims to optimise
the care of patients with sepsis during the first 6
hours from onset of symptoms. It starts with the
Sepsis Six six tasks easily performed by non-
specialist staff, which provide the crucial first
steps in delivering the care bundle:
THE SEPSIS SIX
Give high-flow oxygen
Take blood cultures
Give intravenous antibiotics
Start intravenous fluid resuscitation
Check haemoglobin and lactate levels
Measure accurate hourly urine output
Following the Sepsis Six, the SSC recommends
that patients with persistent hypotension or
increased lactate should be managed with early
goal directed therapy (EGDT). EGDT will require
input from your critical care colleagues or other
senior doctors, but the principles used are
important to recognise and are outlined below.
SSC Management Care Bundle
Following initial resuscitation, the SSC has
recommendations for the next 24 hours of
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SURVIVING SEPSIS CAMPAIGN
SEPSIS RESUSCITATION CARE BUNDLE
Measure serum lactate
Get blood cultures before giving antibiotics
From the time of presentation, give broad
spectrum antibiotics:
within 3 h for emergency department
admissions
within 1 h for non-emergency department,
ICU admissions
In the event of hypotension or lactate
> 4 mmol/l:
deliver an initial minimum of 20 ml/kg of
crystalloid (or colloid equivalent)
apply vasopressors for hypotension not
responding to initial fluid resuscitation to
maintain mean arterial pressure of
65 mmHg
In the event of persistent hypotension
despite fluid resuscitation (septic shock)
or lactate > 4 mmol/l:
achieve CVP of 8 mmHg
achieve central venous oxygen saturation
of > 70%
These tasks should begin immediately and
must be done within 6 h for patients with
severe sepsis or septic shock.
treatment. The Management Care Bundle includes
specialist critical care treatment and strategies
proven to improve patient outcome. Although
outside the remit of the CCrISP course, these
therapies include the use of activated protein C
when indicated, tight glycaemic control and
limitation of ventilatory pressures when using
positive pressure ventilation.
CHAPTER 12 | SEPSIS AND MULTIPLE ORGAN FAILURE
MANAGEMENT OF MULTIPLE
ORGAN FAILURE
Due to the severity of the initial insult or when
there is a persistence of an activated systemic
inflammatory response, a patient may develop
dysfunction or failure of one or more organ systems
(cardiovascular, pulmonary, renal, gut, liver,
haematological, CNS). When 3 or more systems
have failed, the ensuing mortality approaches
80100%. Once one organ system has failed,
others typically follow like a collapsing pack
of cards (see case scenario). It is important to
appreciate the phenomenon of multi-organ failure
and to support each organ system to avoid further
adverse events (e.g. ventilation, haemofiltration/
haemodialysis, inotropic support, nutritional
support, use of blood products).
Respiratory failure may be the result of infection
(often added to pre-existing chronic airway
disease) or adult respiratory distress syndrome
(ARDS). ARDS is a diffuse, inflammatory process,
usually involving both lungs, and is often seen as
part of a sepsis syndrome associated with any
underlying cause. The lungs become waterlogged
due to extravasation of inflammatory fluid and
cells. Patients may develop ARDS quickly,
deteriorating rapidly over a few hours. Pulmonary
signs are often minimal or non-specific: patients
are breathless, becoming progressively tachypnoeic
and hypoxic. A chest X-ray will show bilateral
infiltrates but this may lag behind the clinical
picture. Respiratory support is almost always
needed (usually IPPV) and expert ICU help should
be obtained at an early stage. Suspicion is the
key to diagnosing ARDS.
Cardiovascular failure in MOF results from 3
main factors: (i) loss of peripheral vascular tone
(vasodilatation); (ii) loss of circulating volume
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CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 12.3

When on call, you are asked to review the patient discussed above (Case Scenario 12.2) 72 h following
surgery. She had improved for 48 h and was returned to the ward, but is now breathless and pyrexial
again (38.3C), having been apyrexial since 4 h after surgery. Blood pressure is normal but she is
tachycardic (115 bpm), tachypnoeic (28/min) and poorly perfused. Urine output has fallen off over
the last 4 h to 12 ml in the last hour. The chest seems clear. Her abdomen is distended and quiet.
The stoma has not worked properly yet. The pelvic drain has produced 40 ml serous fluid today only.
You give high flow oxygen (12 l/min) and start a fluid challenge of 500 ml saline stat.
The foundation year doctor had checked bloods and a chest X-ray. Apart from a leukocytosis
(17,000), results are unremarkable. There are no diagnostic features on the chest X-ray. There are
no signs of DVT and prescribed DVT prophylaxis (s.c. heparin and TED stockings) were in place. You
perform a cautious rectal examination but find no obvious abnormality. Blood gases are now
checked and show PaO2 (on FiO2 of 0.6) 11.4 kPa, pH 7.29, BE 7.2. You move the patient to HDU.
When the results come back, you decide that the patient has been acidotic and hypoxic and that
you have barely corrected the hypoxia with the facemask oxygen. After 1000 ml of saline, there
is a little improvement in perfusion, but no change in heart rate and urine output is only 15 ml
in the hour since you were called.
WHAT WOULD YOU DO NOW? WHAT IS YOUR DIFFERENTIAL DIAGNOSIS?
The patient remains breathless and you have neither a diagnosis nor any further intervention of
obvious help at your disposal. You request an urgent review by ICU and, as the patient still seems
underperfused, give a further fluid challenge, while the foundation year doctor checks an ECG
(normal).
The ICU team arrive and assess the patient They share your concern and think ventilation will be
needed transfer is arranged. You inform your consultant, who asks to be kept informed. During
transfer, the patient becomes more breathless and is intubated shortly after arriving in ICU. The
positive pressure ventilation reduces cardiac filling and, despite further fluid loading, inotropes are
required to support the cardiovascular system. Urine output tails off. A chest X-ray shows some
diffuse bilateral shadowing suggestive of ARDS. You update your consultant who comes to examine
the patient. No cause for deterioration has yet been found.
Given the previous operation and the leukocytosis, recurrent abdominal sepsis is suspected. The
patient is too unstable for CT, so repeat laparotomy is arranged and carried out by the consultant.
The bowel is intact but two abscesses are found between loops of small intestine and a left subphrenic
abscess is identified: these are drained and lavaged. More pus is sent for culture.
The patient returns to ICU for full cardiac, respiratory and renal support. The culture result from the
pus taken at the first operation has grown a coliform resistant to prescribed antibiotics but sensitive
to netilmicin. Treatment is changed accordingly and a 7-day course started. The patient slowly
begins to improve over the succeeding 72 hours.

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LEARNING POINTS
Remember the SSC: Prevent, Diagnose, Act
sepsis can progress rapidly an escalating degree of support, often out of working hours,
may be required. Your role is to recognise and treat the many patients with minor sepsis
who respond adequately on the ward, but also to recognise the patient who is not responding
and who needs ICU help
a diagnosis which accounts adequately for any septic deterioration is essential this allows
definitive treatment (source control)
early cultures can help target later treatment the right antibiotic is important.

due to leaky capillaries (hypovolaemia); and (iii)
myocardial depression (pump failure). Arrhythmias
can exert a further effect. Close monitoring of
cardiovascular status is essential to guide treatment
adequately. Fluid resuscitation may prove successful,
although inotropic and vasopressor support is
often required. Many intensivists use noradrenaline
to increase peripheral vascular tone, often in
conjunction with other agents to increase cardiac
contractility.
Renal failure which is common in MOF is often
established during the early stages of the condition
before hypovolaemia is corrected. Circulating
nephrotoxins may compound this. Although
renal function usually improves when the patient
recovers, renal replacement therapy may be
required during the period of MOF and for some
time afterwards. Failure of other systems occurs
(gut, brain, clotting system) may be due to direct
effects of the pathology or to systemic inflammation
and hypoxia. For there to be any prospect of
recovery, the underlying cause or source of sepsis
must be treated.
Nosocomial (hospital acquired) infection is common
in patients treated in ICU and may compound
MOF. The decision to give antibiotics for a
positive culture (e.g. of Pseudomonas spp.) should
be carefully balanced by the presence of a host
response to such bacteria, the site of the potential
infection and the need to avoid superinfection
or antibiotic resistance. Such issues should be
discussed with the microbiologist.
The recognition of the role of endogenous
mediators in sepsis syndrome and the advent of
biotechnology resulted in several, large, multicentre,
randomised trials using monoclonal antibodies or
antagonists to various sepsis mediators including
activated protein C, endotoxin, tumour necrosis
factor and interleukin-1. However, it remains clear
that these treatments are unlikely ever to replace
the established basic principles of management,
although time will tell whether a substantial
adjuvant role can be identified.

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CASE SCENARIO 12.4

The patient again deteriorates overnight, needing increased vasopressors, inotropic support and
oxygen, highly suggestive of sepsis. A full infection screen has been taken by the time you arrive
and the central lines have been changed by your ICU colleagues. There are no clinical features to
suggest recurrent intra-abdominal sepsis: an abdominal CT confirms there is no new intra-abdominal
collection. The patient has had several recent courses of antibiotics and there is no clear best-
guess antibiotic to use.
WHAT IS YOUR DIFFERENTIAL DIAGNOSIS?
6 hours later, the patient is no better and a joint discussion is held between surgeons, ICU staff
and the microbiologist. No cultures are available but fungi were seen on samples from the urinary
catheter and one of the removed central lines. It is decided to start treatment with amphotericin
and fluconazole for presumed fungal sepsis.
After a 4-week course and several other complications, the patient is discharged to the ward.

LEARNING POINTS
Surgical patients on ICU with sepsis and MOF run a roller-coaster course, often with a range
of complications some surgical and some medical. An active surgical input to care helps
manage these effectively.
Multiple courses of antibiotics, gastrointestinal perforation, critical illness and multiple
monitoring lines are all risk factors for fungal sepsis many of these factors pertain in a
majority of surgical patients.
Fungal sepsis may present with obscure signs a failure to progress. Identification of fungi
within the blood, abdomen or urine (or at any 2 other sites) would prompt many intensivists
to discuss antifungal therapy with their microbiologist and surgeon.

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 CHAPTER 12 | SEPSIS AND MULTIPLE ORGAN FAILURE

Established septic shock or MOF is thus really SUMMARY

only treatable by prevention through attention sepsis is a mediator disease
to detail. prevention is better than cure
Pre-operatively, the general health of the patient clinical signs may be obvious, but are
should be optimised (co-existing diseases, nutrition) often covert
and any focus of sepsis should be treated. treatment is much easier at an early stage
Peri-operatively, prophylactic antibiotics should the principles of management are:
be given and surgery executed in a rapid, clean (i) rapid resuscitation to restore oxygenation
and haemostatic manner in order to prevent and perfusion;
complications. Operations should be performed (ii) continued optimal organ support;
electively whenever possible. (iii) diagnosis and eradication of the source
of sepsis and any pus;
Postoperatively, assess clinically and monitor
(iv) judicious and appropriate antibiotic
closely to detect problems at an early stage and
treatment after cultures; and
deal with these quickly and comprehensively. Be
(v) re-assessment to ensure continued progress
alert to occult hypoxia and hypovolaemia. Use
the SSC guidelines, particularly the Sepsis Six,
prophylactic measures such as chest physiotherapy
are a useful starting point in the management
and resume oral intake/enteral feeding at the
of the patient with severe sepsis.
earliest opportunity. Remove lines and tubes as
soon as possible, and employ short courses of
targeted antibiotics. In the event of a septic
complication, adequate resuscitation and early
definitive treatment should reduce the chance of
full-blown sepsis developing.

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182
13
Nutrition in the
surgical patient

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
be aware of the frequency, causes and
importance of inadequate nutrition amongst
critically ill surgical patients
understand the implications of the metabolic
responses to starvation, injury and sepsis for
the provision of nutritional support
know how to assess nutritional status
and devise regimens for nutritional support
comprising macronutrients, trace elements,
vitamins and minerals
choose the most appropriate route for the
administration of nutritional support
recognise and manage the complications
associated with nutritional intervention.
Malnutrition occurs when there is a deficiency
of energy, proteins, vitamins and minerals causing
effects on body function and/or clinical outcomes.
It can occur in surgical patients either as a cause
or as result of the surgical condition.
Malnutrition is a common finding in surgical
patients: as many as 50% of patients on general
surgical wards are reported to have evidence of
protein-energy malnutrition (PEM). Although,
in many cases, these effects may be due to the
nature of the disease process itself rather than
malnutrition, it is important to ensure that,
wherever possible, inadequate nutritional intake
does not add to the likelihood of a poor outcome
in critically ill and postoperative patients.
184
INDICATIONS FOR
NUTRITIONAL SUPPORT
Nutritional support should be considered for all
malnourished patients. Malnourished patients are
defined by NICE as those with:
a BMI of less than18.5 kg/m2
an unintentional weight loss greater than
10% within the last 36 months
a BMI less than 20 kg/m2 and unintentional
weight loss greater than 5% within the last
36 months.
Surgical patients at risk of malnutrition should
also be considered for nutritional support if they
have:
not had, or are not likely to have, significant
oral intake for more than 5 days, or
a poor absorptive capacity, high nutrient losses
or increased nutritional needs due to increased
catabolic rate.
In many critically ill patients (notably those
with SIRS and sepsis), the underlying problem
relates to impaired utilisation of fuel substrates,
rather than an absolute deficiency, and no amount
of externally-added nutrients will reverse the
process which is consuming the bodys reserves.
Efforts must, therefore, be directed to identifying
and treating the underlying cause, including any
source of infection or necrotic tissue.
Nutritional support should be considered for
every surgical patient unable to resume adequate
dietary intake for more than 35 days and in
every critically ill patient, although its benefit
may not be realised until the underlying disease
process settles. If the gastrointestinal tract is
working and access to it can be safely obtained,
enteral feeding should be initiated. It is cheaper,
safer, and has physiological advantages over
alternative methods of support. The barrier function

of the small intestine deteriorates if luminal
nutrients are not provided. This may increase
the ability of bacteria and endotoxins to cross
the intestinal wall, and possibly contribute to the
development of multiple organ failure. The villous
height, which determines the mass and surface
area of the small bowel, also decreases rapidly,
increasing the risk of diarrhoea on resumption
of feeding. This, in turn, may delay introduction
of oral feeding, compounding the situation.
Furthermore, liver dysfunction, hyperglycaemia
and septic complications, especially chest infections,
are significantly less common with enteral feeding
compared to parenteral nutrition.
Nutritional support must be an integral part of
good surgical and critical care support.
Consideration must be given to the duration of
support required. In patients with simple starvation,
considered for elective surgical intervention,
nutritional support needs to be given for a minimum
of 2 weeks pre-operatively before any significant
benefit can be anticipated.
CALCULATING NUTRITIONAL
REQUIREMENTS
Nutrition support should include consideration of:
energy, protein, fluid, electrolyte, mineral,
micronutrient and fibre requirements
any underlying condition (e.g. pyrexia)
the likely duration of need for nutritional support.
Energy requirements can be satisfied in the form
of fats, glucose or protein, which provide: fats, 9.3
kcal/g; glucose, 4.1 kcal/g; and protein, 4.1 kcal/g.
There are several disadvantages in using glucose
as the major energy source, so at least 50% is
provided in the form of fat. Critically ill patients
are often glucose intolerant and excess undergoes
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CHAPTER 13 | NUTRITION IN THE SURGICAL PATIENT
hepatic conversion to lipid causing fatty liver
and derangement of liver function tests. Also,
carbohydrates have a higher respiratory quotient
than fat and protein, producing a greater proportion
of CO2 to O2 consumed, which can increase
ventilatory requirements and contribute to
respiratory dysfunction.
The essential amino acids (e.g. leucine, methionine)
and minerals (zinc, magnesium, etc.), which cannot
be synthesized in the body, must be incorporated
into nutritional support.
A basic nutritional prescription is included in
Table 13.1.
TABLE 13.1
A BASIC NUTRITIONAL PRESCRIPTION
30 kcal/kg/day total energy
0.81.5 g protein/kg/day
(equivalent to 0.150.3 g nitrogen/kg/day)
3035 ml/kg fluid
essential amino acids, adequate electrolytes,
essential minerals and micronutrients
Clearly, critically ill patients will require more
nitrogen in the form of protein, more energy
and probably more fluid. Nutritional support
must, therefore, be calculated on an individual
basis. People who have been ill or malnourished
for some time and who require additional feeding,
should initially not be given their full energy
requirements as they are at risk for developing
refeeding syndrome (see below). It is safe to start
feeding at 50% of estimated protein and calorie
requirements and build up to full requirements
over a 2448 hour period. This only applies to
the energy component of the prescription.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
ROUTES OF ENTERAL FEEDING
SUPPLEMENTARY ENTERAL FEEDING
Supplementation of the diet with sip feeds may
be very useful when patients have a poor appetite
but are able to drink. Sip feeds are therefore
useful in people who can swallow safely but are
malnourished or at risk of malnutrition. Current
sip feeds typically provide 200 kcal and 2 g of
nitrogen per 200 ml and are available in a variety
of flavours. They may be useful in enabling
patients to make the transition back to a full diet
and there is some evidence to suggest that they
may reduce hospital stay and increase the speed
of postoperative recovery. However, they are often
used to replace, rather than supplement, food
intake and, despite manufacturers best efforts,
many patients still find them unpalatable. Offering
sip feeds chilled and in a variety of flavours can
help, along with encouraging nursing staff to
offer normal oral nutrition at mealtimes in
addition to supplements. Multivitamin and mineral
supplements can be used to ensure there are
sufficient micronutrients in the diet (Table 13.2).
186
TABLE 13.2
BASIC RULES FOR ENTERAL NUTRITION
Enteral nutritional support should be
considered when:
spontaneous oral intake is inadequate
the proximal small intestine is intact
and functional
stimulation of secretory function does not
clearly worsen the condition being treated
(e.g. proximal small bowel fistula).
Contra-indications (relative and absolute)
include:
complete small bowel obstruction
inadequately treated shock states (may
be associated with a risk of intestinal
ischaemia)
severe diarrhoea (low rate of feeding
may be continued as it may improve
absorptive surface)
proximal small intestinal fistulae
severe pancreatitis (unless fed distal
to pancreas).
NASOGASTRIC FEEDING
Feeding through a nasogastric tube is the easiest
means of enteral feeding, but is reliant on the
adequacy of gastric emptying, which is one of
the last aspects of gut function to recover after
an operation or major insult. High gastric residuals
and gastric distension predispose to vomiting or
regurgitation and aspiration. Any impairment of
consciousness greatly increases this risk. Keeping
the patient at least 15 head up may reduce this
risk significantly.

Judging when gastric emptying is adequate can
be difficult. In the fed state, the stomach can
produce up to 2500 ml of secretions (in addition
to receiving 1500 ml of saliva). The normal gastric
residual volume is between 50100 ml, which
represents the equilibrium between secretion,
and emptying plus absorption. Continuous passive
drainage or suction through a conventional
wide-bore nasogastric tube may lead to a large
cumulative total over 24 hours even in the face
of normal gastric emptying, because the gastric
residual is replaced as quickly as it is removed.
Pinning the bag up at shoulder height or spigotting
the tube and aspirating at 2-, 4- or 6-hourly
intervals will give a better indication of whether
the stomach is emptying adequately. Most stresses
and illnesses, plus some drugs, increase gastric
residual volume, but may not necessarily lead to
a degree of impaired emptying that would prevent
feeding. Feeding can be commenced through a
standard, large-bore nasogastric drainage tube,
but a fine-bore tube is better tolerated once the
need for drainage has passed. Aspiration of gastric
fluid through a fine-bore tube is much more
difficult, and confirmation of tube position is
mandatory because of the devastating consequences
of instilling feeding solution into the lung (as
highlighted by the National Patient Safety Agency).
Tube position must be confirmed either by checking
the pH of gastric contents aspirated from a
large-bore tube, or radiographic confirmation.
NASOJEJUNAL OR NASODUODENAL FEEDING
Where gastric emptying remains a problem or
direct intragastric feeding is undesirable, such as
in severe pancreatitis, a weighted tube should be
used and guided into the proximal small intestine.
If undergoing surgery, this can be placed intra-
operatively, but other options include the use of
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CHAPTER 13 | NUTRITION IN THE SURGICAL PATIENT
fluoroscopy to advance the tube beyond the
pylorus, endoscopic placement or the use of
specially designed tubes that are propelled
distally by peristalsis. Prokinetic drugs such as
erythromycin and metoclopramide that promote
gastric motility may also be given to encourage
forward movement of the tube beyond the pylorus.
TUBE ENTEROSTOMY
Where patients are undergoing laparotomy,
consideration should be given to the insertion
of a tube enterostomy as a planned part of the
procedure. For example, tube jejunostomy
should be considered in patients undergoing
oesophagectomy, total gastrectomy or
pancreaticoduodenectomy or a laparotomy for
abdominal trauma. For other patients, insertion
of feeding tubes should be considered when it is
clear that enteral nutritional support is indicated
and is going to be required for more than 6
weeks. Tube gastrostomy can be fashioned using
either the Stamm (pure-string suture) or Witzel
(seromuscular tunnel) techniques. Tube jejunostomy
can also be accomplished using a catheter
introduced over a fine needle, passed submucosally
before entering the bowel. In all cases, the bowel
should be sutured to the abdominal wall deep to
the site at which the catheter passes through.
Minimal access techniques can also be used.
Percutaneous endoscopic gastrostomy (PEG) and
transgastric jejunostomy are appropriate in the
management of patients in whom laparotomy is
not indicated but who need enteral nutritional
support for a prolonged period.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

TABLE 13.3

COMPLICATIONS OF PEG FEEDING

Condition Action Incidence

Infection at PEG site Keep clean and dry. If pain pus, swab and treat 4%
with antibiotics

Mechanical problems 4%
Blockage Flush with saline
Accidental removal Keep track open with balloon, PEG or Foley catheter
Peritonitis If pain, stop feed, arrange PEG-O-Gram, inform seniors 2%
Aspiration pneumonia 1%

PERCUTANEOUS ENDOSCOPIC
GASTROSTOMY (PEG) FEEDING
PEG is an alternative method to provide direct
tube enterostomy feeding (Fig. 13.1). The technique
involves insertion of a guide-wire through the
stomach wall under local anaesthesia and
endoscopically guided insertion of the PEG through
the abdominal wall over the guide-wire. PEG
feeding is particularly useful following head
injuries, for oropharyngeal malignancy and for
some forms of intestinal failure. It is not suitable
for patients with intestinal obstruction, ascites Figure 13.1 PEG tube for enteral feeding.
or undergoing peritoneal dialysis. There are
complications specific to PEG feeding (Table 13.3). is less than 200 ml, this is generally returned to
the stomach and the rate of feeding increased. If
INITIATION OF ENTERAL FEEDING there is reason to believe that absorptive capacity
A useful regimen in patients with an otherwise will be a problem (for example, with prolonged
normal gut is to start at 20 ml/h for 6 hours, then disuse leading to villous atrophy or significant
increase by 2030 ml/h and repeat the process. small bowel resection), the progression to full
If gastric tubes are used, aspiration to assess the feeding may need to be much more gradual to
gastric residual can be performed before each prevent diarrhoea. Diarrhoea is one of a number
increase, bearing in mind that some aspiration of of potential complications of all modes of enteral
gastric contents is normal. If the volume aspirated feeding (Table 13.4).

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a degree of enteral intake or introducing it soon

TABLE 13.4 after surgery, even if it falls well short of meeting
total nutritional needs. It is important to rule out
COMPLICATIONS OF ENTERAL FEEDING
infection with Clostridium difficile or other
Related to intubation of gastrointestinal tract bacterial dysenteries before treating with agents
Fistulation to slow gut transit. Such agents include loperamide,
Wound infection codeine or kaolinpectin mixtures, and can be
Peritonitis very effective, especially after extensive small
Displacement and catheter migration bowel resection.
(including small bowel obstruction)
A protocol for the management of enteral nutrition
Blockage of tube
associated diarrhoea is given in Fig. 13.2.
Related to delivery of nutrient to
gastrointestinal tract
Aspiration and hospital-acquired pneumonia
Exclude infectious causes
(especially if feed contaminated) Send stool for culture, including C. Difficile toxin
Feed intolerance Send feed for culture
Diarrhoea

Reduce feeding load on the gut

On a daily basis, surgeons should review the Reduce rate of delivery of feed (try 20 ml/hr)
indications for feeding, nutritional requirements Consider jejunal rather than gastric feeding
and the chosen route of supplementation. In In patients with short bowel, consider omeprazole
particular, patients receiving parenteral nutrition to reduce gastric hypersecretion

should be switched to the enteral route as soon

as gut function returns or underlying abdominal
problems settle. Treat diarrhoea empirically

MANAGEMENT OF DIARRHOEA
Diarrhoea can be a major problem in enterally Other measures (unproven)
fed patients and can be multifactorial. The Consider use of fibre or glutamine-containing feeds
Consider IV albumin if low albumin thought to
commonest identifiable cause is concomitant be contributing to malabsorption
administration of antibiotics, which leads to
de-population of the normal gut flora, and also
has a direct irritant effect. If the antibiotics can
Figure 13.2 Protocol for the management of enteral nutrition
be stopped, the diarrhoea will usually resolve associated diarrhoea.
rapidly. Other contributory factors include loss
of intestinal absorptive surface because of villous
atrophy or resection. The effect of villous
atrophy can be minimised by maintaining

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
PARENTERAL NUTRITION
Total parenteral nutrition (TPN) can be defined
as the provision of all nutritional requirements by
the intravenous route alone. NICE has produced
guidelines on artificial nutritional support,
emphasising the careful balance between potential
risks and benefits in all patients. Surgical conditions
associated with a need for TPN are listed in Table
13.5, though the only absolute indication is the
presence of an enterocutaneous fistula.
If possible, a dedicated line should be used for the
administration of TPN. Due to the high osmolality
of the mixture, TPN must be given into a central
vein. In many hospitals the peripheral route to a
central vein (peripherally inserted central line or
PICC line) is preferred. Alternatively, a central line
is inserted in the subclavian vein, or internal
jugular vein tunnelled to an infraclavicular
position to reduce infection risk. The tip of the
line should be screened into the distal superior
vena cava because this promotes maximal mixing
of the feeding solutions with venous blood,
reducing the risk of catheter-associated thrombosis.
Intravenous feeding via the femoral vein should
be avoided because of the high incidence of line
infection and other catheter-related complications.
The exit site should be protected carefully with an
occlusive dressing and full aseptic technique used
when dressings are changed or the line handled.
190
TABLE 13.5
INDICATIONS FOR TOTAL PARENTERAL
NUTRITION IN SURGICAL PATIENTS
Critical illness
Where enteral feeding is not established
within 5 days
Obstruction of the gastrointestinal tract
For example, patients with proximal
small bowel obstruction which cannot
be immediately relieved and who require
pre-operative feeding
Short bowel syndrome
Patients with < 300 cm of functional small
intestine usually require at least temporary
TPN. In many cases, adaptation will
eventually permit enteral nutrition alone.
Patients with less than 100 cm of small
bowel generally require life-long TPN
Proximal intestinal fistulae
May facilitate fistula closure. Use where
enteral intake is restricted
Refractory inflammatory disease of the
gastrointestinal tract
Inability to use the gastrointestinal tract
for other reasons
For example, pancreatitis with
pseudocysts/ abscess where enteral
nutrition is not tolerated

COMPLICATIONS ASSOCIATED WITH TPN
The potential severity of line sepsis should not
be underestimated and a high degree of suspicion
maintained if a patient develops signs of sepsis
or unexplained clinical deterioration. When a
multi-lumen catheter has to be used, one channel
should be preserved solely for TPN. The most
common source of infection in catheter-related
sepsis is the hub of the catheter. Strict aseptic
technique is essential at all times, cleaning the
hub with chlorhexidine whenever used. Three-
way taps should not be used when TPN is being
infused, and unless catheter-related sepsis is
suspected, the catheter should not be used to
draw blood samples.
Other catheter-related complications and
metabolic disturbances associated with TPN
are shown in Table 13.6. Also, fluid overload
can occur, usually as a result of inappropriate
continuation of other intravenous fluids, and
electrolyte disturbances are relatively common
though are usually predictable and preventable.
Refeeding syndrome is a rare and often preventable
complication, which causes confusion and weakness
associated with electrolyte disturbances. Criteria
for determining people at high risk of developing
refeeding problems have been devised by NICE,
including low BMI, duration of reduced intake,
degree of weight loss and electrolyte abnormalities.
In those at risk, feeding should be introduced
gradually over 48-72 hours.
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CHAPTER 13 | NUTRITION IN THE SURGICAL PATIENT
TABLE 13.6
COMPLICATIONS ASSOCIATED WITH
THE PROVISION OF TPN
Catheter-related
Mechanical blockage, central vein
thrombosis, migration, fracture,
dislodgement
Infective exit-site infection, line sepsis,
infective endocarditis
Metabolic
Hyperglycaemia too much glucose
infused. Occasionally seen in severe sepsis,
treat with insulin
Deranged liver function cause unclear
but may relate to biliary stasis, enzyme
induction from amino acid imbalance and
excessive calorie administration, with fat
deposition in liver
Hypoglycaemia too rapid cessation of
glucose infusion
Hypertriglyceridaemia too much lipid
infusion
Hyperchloraemic acidosis too much
chloride in nutrient solution
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
ADVANCED NUTRITIONAL
THEORY AND PRACTICE
METABOLIC RESPONSE TO STARVATION,
INJURY AND SEPSIS
Malnutrition in surgical patients may occur
from starvation due to fasting, but surgery and
sepsis also cause a systemic metabolic response
that contributes significantly to the clinical
picture and to nutritional management.
Feeding and fasting
In health, feeding replenishes fuel stores and the
oxidative metabolism of fuel generates energy
for metabolic processes. The normal daily
resting energy expenditure of a 70 kg man is
approximately 1800 kcal. The brain uses
carbohydrate as its sole fuel in the fed state and
requires approximately 100 g of glucose per day.
Any glucose not consumed by the brain is used
to restore liver carbohydrate stores (glycogenesis)
and the rest is converted to fat (lipogenesis).
Amino acids are used to replenish those lost in
the normal daily turnover of protein (including
skeletal and cardiac muscle, liver and intestinal
structural proteins and liver export proteins such
as albumin) while the rest are metabolised in the
liver, converting the carbohydrate component
into fuel (gluconeogenesis) and the nitrogenous
component to urea for excretion.
Lipid is stored primarily as triglyceride within
adipose tissue. Lipid cannot be directly converted
into either amino acids or glucose.
The hormonal environment associated with recent
feeding (high insulin levels and low glucagon
levels) allows the storage of nutrients as described
above.
192
Fasting leads to a number of changes in the
utilisation of energy sources within the body
(Table 13.7). After a short (12-hour) fast, all of
the food ingested during the previous meal is likely
to have been utilised. The major source of glucose
for the brain shifts to glycogen stored in the liver
(of which there is approximately 200 g). This
breakdown of glycogen to provide glucose
(glycogenolysis) is facilitated by decreasing insulin
levels and increasing glucagon levels. Though
skeletal muscle contains a larger amount of
glycogen (500 g), this cannot directly contribute
to the provision of glucose for other tissues.
Instead, glucose is converted to lactate within
muscle, which is exported to the liver for conversion
to glucose (Cori cycle). Glucose is also converted
to lactate within haemopoietic tissues.
Muscle derives approximately one-third of its
energy from the oxidation of glucose and the rest
from the oxidation of fatty acids derived from
the breakdown of fat in adipose tissue (lipolysis).
Muscle protein breakdown begins to contribute
amino acids (alanine and glutamine) for hepatic
gluconeogenesis. After about 48 hours of starvation,
approximately 75 g of muscle protein is being
broken down each day. Glycerol and triglycerides
from fat depots are used to make up the shortfall
in energy requirements and fatty acids provide
the main metabolic fuel for many tissues.
With more prolonged fasting, a series of
metabolic adjustments develop in order to
preserve body protein. For example, the liver
gradually increases its capacity to produce ketone
bodies from fatty acids. The brain adapts to use
ketone bodies, reducing muscle breakdown by
up to 55 g/day and preserving vital muscle and
visceral protein. This is maintained as long as
ketone body production persists, fuelled by

the availability of fat stores. While absolute rates
of protein breakdown decrease (in contrast to
critical illness), the reduced anabolism which
results from the lack of substrate leads to a net
catabolism. These metabolic adjustments are
associated with low levels of insulin and high
plasma glucagon concentrations. A gradual
decline in the conversion of inactive thyroxine
(T4) to active triiodothyronine (T3) results in
a fall in energy requirements to approximately
1500 kcal/day.
TABLE 13.7
METABOLIC RESPONSES TO FASTING
Insulin levels fall
Glucagon levels rise
Hepatic glycogenolysis
Muscle and visceral protein catabolism
Hepatic gluconeogenesis
Lipolysis
Ketogenesis sparing 55 g/day of muscle
protein
Fall in metabolic rate
(typically to 1500 kcal/day)
Metabolic responses to surgery
Many of the metabolic responses to surgery,
or injury in general, can be understood on the
basis of the associated hormonal alterations (see
Table 13.8). Release of noradrenaline, adrenaline,
glucagon, growth hormone and cortisol occurs.
Initially, plasma insulin levels fall but may later
rise to levels in excess of those normally
encountered for a given glucose concentration.
The normal anabolic effects of insulin are
impaired (insulin resistance). In addition, there
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CHAPTER 13 | NUTRITION IN THE SURGICAL PATIENT
is a relative increase in glucagon concentration.
The hormone response increases with the severity
of trauma and its effect is to increase the
availability of fuel for metabolic processes.
There is a modest increase in the metabolic rate
to approximately 2000 kcal/day and lipid is the
major fuel used for energy production. Muscle
protein breakdown increases and glycogenolysis
and gluconeogenesis result in an increased
availability of glucose. This is used primarily by
the brain, white blood cells and healing tissues.
Glutamine is also released from skeletal muscle
and, under conditions of stress, appears to be
essential for the normal functioning of cells in
the small intestine and immune system.
As the stress response reduces and insulin
resistance falls, there is a shift towards a net
anabolism, making up the lost reserves of protein
and energy. This usually coincides with the
resumption of eating and of increasing mobility,
both of which are required to restore muscle mass.
TABLE 13.8
METABOLIC RESPONSE TO INJURY
Modest rise in metabolic rate (and,
therefore, energy expenditure) typically
2000 kcal/day
Counter-regulatory hormone response
adrenaline, noradrenaline, cortisol,
glucagon and growth hormone
Resistance of tissues to effects of insulin
Glucose intolerance
Preferential use of lipid as energy source
Exaggerated gluconeogenesis and breakdown
of muscle protein, despite feeding
Loss of adaptive ketogenesis
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Metabolic response to sepsis
The changes in metabolism that develop with
the onset of sepsis are complex and are an
exaggeration of those described after injury
(see Table 13.9). The key changes are a markedly
increased metabolic rate (hypermetabolism) and
rate of protein breakdown. There may be marked
glucose intolerance with the development of a
diabetes-like state. Despite this hyperglycaemia,
glucose utilisation and storage are impaired and
the septic patient has a greater reliance on fat
as a metabolic fuel for energy production. There
is frequently marked fluid retention. The rate of
protein breakdown may reach 250 g/day. Muscle
and visceral protein is thus consumed for the
generation of glucose, despite the frequently
elevated plasma glucose concentration. Although
some of this exaggerated muscle protein breakdown
might be due to the hormonal environment,
the release of cytokines such as interleukin-1,
interleukin-6 and tumour necrosis factor may
also be implicated.
TABLE 13.9
METABOLIC RESPONSE TO SEPSIS/SIRS
More marked increase in metabolic rate,
hence energy expenditure (22002500
kcal/day)
Exaggerated gluconeogenesis, protein
catabolism and muscle wasting
Marked fluid retention
Insulin resistance common and may
be severe
194
ASSESSMENT OF NUTRITIONAL STATUS
Protein-energy malnutrition (PEM) often goes
unrecognised in surgical patients, despite its
prevalence and adverse prognostic implications.
An assessment of the patients nutritional status
should form part of every physical examination.
Gross degrees of malnutrition such as obvious
wasting are easily recognised but more subtle
degrees of deficit may not be, particularly in the
obese patient. Body weight standardised to height
as BMI is probably still the most useful measure
of nutritional status.
Anthropometric measurements (e.g. measures of
skinfold thickness and midarm circumference)
allow estimation of muscle mass (protein reserves)
and fat mass (energy reserves) but are often
inaccurate, particularly in critically ill patients.
Functional tests, including hand grip and respiratory
muscle strength are predictive of the loss of
muscle mass loss but have limited clinical use.
Formulas to assess energy requirements, such
as the HarrisBenedict equation, rely on poorly
substantiated correction factors for various
clinical conditions such as sepsis or burns, and
tend to overestimate energy expenditure. The
most accurate way (albeit still with substantial
variability) to assess energy expenditure in the
clinical setting is by indirect calorimetry, using
a bed-side metabolic cart. This technique, which
involves measurement of oxygen consumption
and CO2 production requires expensive equipment
and is generally beyond routine clinical use.
Laboratory tests which are claimed to reflect
malnutrition such as albumin principally measure
how sick the patient is, rather than measures of
inadequate nutritional intake per se. For example,
in simple starvation, serum albumin concentrations
remain unaltered for nearly 6 weeks and begin
 CHAPTER 13 | NUTRITION IN THE SURGICAL PATIENT

to fall just before death. In contrast, in sepsis,

the serum albumin concentration commonly falls TABLE 13.10
to below 20 g/l within a couple of days or even
BLOOD TESTS IN THE MONITORING OF
hours, principally due to re-distribution into the
NUTRITIONAL STATUS IN STABLE
interstitial space.
PATIENTS (IN THE UNSTABLE PATIENT,
Laboratory investigations to look for the presence THE FREQUENCY WILL BE INCREASED)
of associated trace element, vitamin and electrolyte
Daily
deficiencies, however, may be of value.
Full blood count
Measurement of standard electrolytes, along with
Glucose (may need feeding and
magnesium, calcium and phosphate will enable
fasting samples)
demonstration of major electrolyte abnormalities.
Urea, creatinine and serum electrolytes
Interpretation of sodium and potassium balance
can be difficult in critically ill patients, especially Weekly
in the presence of large gastrointestinal losses Magnesium, calcium, phosphate
(e.g. in association with an intestinal fistula or a Chloride
proximal stoma), but they should be checked on Albumin
a daily basis (see Table 13.10). Bilirubin
Transaminases
While an assessment of the degree of metabolic
Gamma glutamyl transpeptidase
stress to which the patient is being subjected can
Alkaline phosphatase
be made, the most important step in nutritional
Prothrombin time
assessment is to consider the need for nutritional
support in every patient based on the underlying Twice monthly
diagnosis, recent events and the likely time to Vitamin B12 and folate
restoration of adequate nutritional intake. Iron and iron-binding capacity
Adequate nutritional intake does not automatically Copper, zinc, selenium
occur when the patient is first allowed to commence Pre-albumin, transferrin
oral fluids!

INTESTINAL FAILURE
Intestinal failure can be said to exist when the
functioning intestinal mass of a patient is reduced
below the minimal amount necessary for the
adequate digestion and absorption of food.
Like renal failure, intestinal failure is the end
result of many different disease processes. It is
also a continuum ranging from temporary mild
dysfunction to complete and irreversible failure
needing chronic replacement therapy.

195
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
At one extreme, intestinal failure may be an acute
reversible problem (e.g. small bowel obstruction);
at the other, a chronic condition resulting from
an irreversible loss of gut mass (e.g. mesenteric
vascular occlusion). Intestinal failure is a clinical
diagnosis based on a history and examination,
laboratory investigations and, in some cases,
radiological investigations. Establishing a diagnosis
of intestinal failure is important because attempts
to provide enteral nutritional support alone are
likely to be ineffective and early parenteral nutrition
should be considered, possibly with referral to
a specialised unit.
196
SUMMARY
Nutritional support of the critically ill is a
frequently neglected, but integral, part of the
delivery of surgical care. Just as the support of
the cardiovascular and respiratory systems of
critically ill patients is based on an understanding
of the altered physiology associated with
disease, nutritional intervention is based on an
understanding of the metabolic processes in the
critically ill. The ultimate goals of nutritional
support in the surgical patient are to ensure that
the patient is optimally prepared for the stress
of a surgical procedure and that recovery, even
in the face of complications, is associated with
minimal depletion of body stores. Use the
expertise available to you on the surgical and
high dependency wards, from nursing staff,
dieticians and dedicated nutritional teams.
think about nutrition in every patient
assess status and nutritional requirements
select the optimum route
check that delivery is successful by monitoring
the response.
14
Pain management

197
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the effects and risks of
inadequate analgesia
learn to function as a member of a
multidisciplinary team providing analgesia
in the critically ill patient
understand your role in the management
of acute pain throughout the continuum of
surgical care from the general ward through
to HDU/ICU
acquire the knowledge to decide on
the appropriate method of analgesia and
the skills necessary for your role in its
deployment
be aware of the systemic effects of
analgesia and the complications of analgesic
techniques.
INTRODUCTION
Nociception is the name given to the reception
of a noxious or unpleasant stimulus and its
conversion into an impulse transmitted through
a sensory nerve. Pain refers to the perception of
that sensation in the CNS and its recognition as
unpleasant. Suffering is the emotional response
that makes one miserable and is associated with
the severity of the pain and its duration.
Society relies on doctors to provide relief of
pain and suffering. It is important for all doctors
to have a fundamental understanding of pain
198
including how it is generated and perceived.
As a member of the surgical team, you will look
after patients presenting with primarily painful
conditions and will encounter pain produced
by surgical operations and interventions.
Safe and effective management of acute pain is
an integral part of surgical practice. Although
the physical status of the patient, the degree of
trauma and the available techniques may be
very different, the principles involved are similar
whether the patient is recovering from major
surgery on a general ward or being managed
on an HDU or ICU.
Good quality analgesia is essential for humanitarian
reasons alone: there are also compelling medical
reasons for its provision. Inadequately controlled
pain increases sympathetic outflow leading to
an increase in heart rate, vasoconstriction and
increased oxygen demand, particularly in the
myocardium where it may contribute to ischaemia.
It may impair lung function; abdominal and
thoracic procedures almost always lead to impaired
respiratory function because the pain induced by
movement inhibits coughing and diaphragmatic
function leading to atelectasis/pneumonia. The
patient who has adequate analgesia is able to
mobilise and this will reduce the incidence of
deep vein thrombosis, improve respiratory function
and improve general psychological well being.
It should also be recognised that pain
postoperatively may be caused by a developing
surgical complication.
However, a degree of pain is not always bad.
Pain causes people to rest and protect injured
tissue, preventing further damage and allowing
healing.
 CHAPTER 14 | PAIN MANAGEMENT

PRINCIPLES OF required. Any patient who has escalating analgesic

ACUTE PAIN MANAGEMENT
The realistic aim of pain relief is not to abolish
pain in the postoperative period totally but to
ensure that patients are comfortable and have
return of function with a more rapid recovery
and rehabilitation. There are several important
principles relevant to the provision of good
quality pain relief.
PREVENT
The single most important step we can take
in alleviating pain is to prevent the factors
that produce it. Avoiding tension during surgical
closure may help, as may preventing drains
or tubes from pulling on sutures or relieving
urinary retention.
The use of drugs preventing the development of
pain is more effective than treatment of existing
established pain. This is the concept of pre-emptive
analgesia. In practical terms, this means that local
anaesthetic drugs or other analgesic agents should
be given prior to surgical trauma rather than
afterwards.
RECOGNISE NEW PROBLEMS
It is critical that trainee surgeons are able to
recognise when a patients pain has altered to
a point where an alternative explanation is
requirements needs to be assessed with a high
degree of suspicion (see Case Scenario 14.1).
Ischaemia is a common trap, as are bleeding,
anastomotic leakage and compartment syndrome.
Breakthrough pain in a patient who previously
had effective analgesia should be treated as a
surgical complication until proven otherwise.
MANAGE EXPECTATION
The two most powerful forces in play during pain
management are the expectation of the patient
and that of the healthcare staff. If either believe
that the patient will be in severe pain, the outcome
will tend towards poorer mobilisation and poorer
outcomes; if both believe the converse, the outcome
is likely to be fewer complaints and more rapid
mobilisation.
Pre-operatively, patients should be told to expect
significant pain in proportion to their condition.
They should also be told that pain can be
controlled by various means and that they will not
be allowed to suffer. If distressed by their pain, or
if pain is inhibiting their breathing or their ability
to cough, a change in technique will be required!
SURGICAL CONSIDERATIONS
Upper abdominal incisions are associated
with considerably more pain, more pulmonary

CASE SCENARIO 14.1

A 75-year-old man has worsening abdominal pain 3 days after low anterior resection. He is requiring
continued high-dose PCA morphine and is now nauseated and vomiting with a tender abdomen.
An anastomotic breakdown and collection in the abdomen needs to be excluded as the patient should
be having decreasing analgesic requirements by this time. The nausea and vomiting may be due to
obstruction not opiate. This patient needs a full clinical assessment to deduce the cause of deterioration
and increased analgesia requirement.

199
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
disturbance and more difficulty effecting adequate
analgesia than lower or transverse abdominal
incisions. The choice of site and type of incision
is therefore important in the sick patient who has
limited respiratory reserve.
Laparoscopic surgery is considerably less traumatic
and so less painful during the postoperative course.
Postoperative pain management will be aided
by the use of local anaesthetic infiltration at the
time of surgery or by specific local and regional
anaesthetic techniques. Epidural infusion analgesia
is the most commonly used of these techniques;
other examples include caudal blocks for perineal
surgery, intercostal blocks for cholecystectomy,
and ilio-inguinal blocks for lower abdominal
incisions. Upper and lower limb surgery can have
major nerve blocks or plexus blocks to provide
postoperative analgesia.
THE ROLE OF THE SURGICAL
TRAINEE IN THE MULTIDISCIPLINARY
ACUTE PAIN TEAM
The provision of postoperative pain relief has
always been hindered by confusion about whose
responsibility it is to perform this function.
Traditionally, postoperative analgesia has been
prescribed by the anaesthetist, administered by the
ward nurses and supervised by a junior surgical
trainee. The Joint College Working Party Report
on Postoperative Pain recommended that each
major hospital should have a multidisciplinary acute
pain team consisting of surgeons, anaesthetists,
nursing staff and pharmacists. With increasingly
sophisticated methods of analgesia being used, it
is vitally important that the surgical trainee liaises
with the other members of the team and is aware
of protocols and guidelines relating to acute pain
management in the hospital.
200
PRACTICE POINT
As the clinician likely to be contacted first
in the case of a surgical patient becoming
critically ill, the surgical trainee must
establish if:
(i) pain is related to a surgical complication;
(ii) poor pain relief is contributing to the
patients lack of progress; and
(iii) the method of analgesia is contributing to
the patients deterioration.
PATIENT ASSESSMENT
AND MANAGEMENT
IMMEDIATE MANAGEMENT
In the critically ill patient in pain, patient
assessment is vital. It should follow the same
CCrISP system of assessment as in any other
circumstance.
Airway
Start at the beginning by checking that the
patient has a patent airway. Over sedation
secondary to opioid drugs may be associated
with episodic airway obstruction. This is
particularly marked in patients who are elderly,
obese, have a history of obstructive sleep apnoea
(OSA) or who have had surgery to the head or
neck. It may be exacerbated by the administration
of other sedative drugs such as benzodiazepines.

PRACTICE POINT
Episodes of airway obstruction and resultant
hypoxaemia often persist for 23 nights after
major surgery. Supplemental oxygen should
be continued for at least 72 hours in high-risk
patients recovering from major surgery who
receive any form of opioid analgesia (including
PCA and by the epidural route).
Breathing
Check the respiratory rate, pattern and depth of
breathing. Is your patients respiratory function
impaired by inadequate analgesia? Can he or she
cough and expectorate properly to avoid problems
later? The rational use of opioid analgesia has
always been limited by the fear of drug-induced
respiratory depression. A much more common
problem is the patient slowly slipping into respiratory
failure due to poorly controlled pain which is
inhibiting movement and the ability to cough.
PRACTICE POINT
Respiratory rate is a late and unreliable
indicator of opiate-induced respiratory
depression. Sedation levels are a more sensitive
indicator of impending opioid overdosage.
Severe hypoxaemia may occur in the presence
of normal or usually raised respiratory rates.
Poorly relieved pain, particularly in upper
abdominal surgery is a major cause of failure
to cough, sputum retention and hypoxaemia.
Remember pulse oximetry oxygen saturations
are not a good guide to respiratory function,
only to oxygenation.
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CHAPTER 14 | PAIN MANAGEMENT
In the assessment of the critically ill patient
in pain, it is therefore essential to assess the
adequacy and depth of the respiratory pattern as
well as respiratory rate, and to check the patients
ability to cough. Investigations including ABG
analysis and continuous pulse-oximetry can
be useful adjuncts to clinical findings when
assessing a patients respiratory adequacy
(see Case Scenario 14.2).
Circulation
Tachycardia should not automatically be assumed
to be caused by pain there is commonly an
underlying cause.
A persistent tachycardia or hypertension caused
by inadequate analgesia may potentiate the
development of myocardial ischaemia, particularly
in the patient who is already hypoxaemic.
A common clinical problem is the differential
diagnosis of hypotension occurring in the
post-surgical patient. This may be due to any
cause of shock, from simple hypovolaemia due
to inadequate fluid input or bleeding, through
cardiac failure due to CCF, ischaemia and
infarction or arrhythmias and septic shock.
The patient may also be receiving epidural
analgesia and this may cause added confusion
as to the cause of hypotension, due to the relative
hypovolaemia secondary to vasodilatation.
Patients with sympathetic blockade are very
sensitive to inadequate volume replacement and
care must be taken in these patients to replace
fluid losses immediately.
This requires meticulous attention to the
maintenance of accurate fluid balance charts,
measurements of losses from surgical drains and
a high index of suspicion for concealed losses.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

FULL PATIENT ASSESSMENT

PRACTICE POINT
Persistent hypotension and tachycardia in
the post-surgical patient may be due to any
cause of shock. All types of shock need to
be considered, investigated and excluded.
Epidural analgesia should not be assumed
automatically to be the cause of hypotension.
Disability
It is important to assess whether the method of
analgesia is contributing to the patients clinical
deterioration. Particular attention should be paid
to the patients level of consciousness as
decreasing conscious level is an early indicator
of opioid toxicity.
Chart review
If pain relief is felt to be contributing to the
patients deterioration, the drug charts should be
reviewed with the following questions in mind:
is effective analgesia prescribed?
is effective analgesia being given?
is the treatment appropriate for this patient?
The recorded pain and sedation scores should be
reviewed and the scores repeated (see below).
History and systemic examination
The contribution of pain to the patients general
condition should be ascertained during your full
patient assessment.
Behavioural observations
Assessment of pain by hospital staff is usually
based on the patients outward response, or pain
behaviour. Verbal complaints, facial expression,
restriction of mobility and changes in heart rate
and blood pressure are used intuitively to build an
impression of how much pain a patient is suffering.
While these are often good predictors of pain, it is
important to realise that, in some individuals,

TABLE 14.1

PAIN SCORING SYSTEMS

Verbal rating scale Is your pain: 0, absent; 1, mild; 2, discomforting; 3, distressing;

4, excruciating
Numerical rating scale Which number describes your pain: 0, no pain; 10, worst imaginable
Visual analogue scale No pain to Worst imaginable
Functional assessment Can you move? Can you cough?

202

such assessments may be quite wrong and we
may significantly under- or over-estimate the
level of suffering.
Severity scoring systems
The effectiveness of assessment of analgesia will
be vastly increased if simple reproducible pain
scoring systems are used. These systems emphasise
restoration of function by assessing pain scores
during movement and when coughing. (Table
14.1.) Pain scores should be recorded when the
patient is taking deep breaths, coughing and on
movement otherwise the score may be falsely low.
PRACTICE POINT
Pain scoring in the patient recovering from
major surgery should be as performed routinely
along with measurement of cardiovascular
and respiratory parameters.
Increasing pain scores should alert you to
potential complications.
Investigations
Investigations assessing respiratory function are
frequently used when assessing the adequacy of
analgesia. Serial ABG analysis and chest X-rays
are often used to demonstrate trends in respiratory
capacity and sputum cultures are essential when
planning antibiotic therapy. Remember that pulse
oximetry only tells you about oxygenation not
overall respiratory function the reading of
saturation should be interpreted in the context of
inspired oxygen concentration and respiratory rate.
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CHAPTER 14 | PAIN MANAGEMENT
Decide and plan
If pain relief is adequate and the patient is
improving then continue and review. If pain
relief is inadequate determine why:
is it due to failure of the method of analgesia?
is it due to incorrect implementation of the
method chosen?
is it due to the development of a surgical
complication?
Pain relief should be considered as an integral
part of the patients total care. In certain situations,
the method of analgesia may determine whether
the patient has a smooth postoperative course
or becomes critically ill. In a patient who has
pre-existing chest disease, for example, the analgesic
technique chosen when an upper abdominal
incision is planned may determine whether a
period of postoperative ventilation on an ICU is
required or not.
TECHNIQUES AVAILABLE FOR
THE MANAGEMENT OF ACUTE PAIN
It is important for all those involved in the delivery
of pain services to understand the range of
techniques available. At one end of this spectrum
is the administration of single analgesic agents,
often administered orally, to a patient in mild
discomfort. As the intensity of pain increases,
there is a need for an increased response from
those providing the pain relief. In some cases,
increased analgesic requirements may be met by
increasing the dose or potency of the drugs used.
Other situations will demand the use of more
sophisticated regimens. Combinations of methods
and agents may be needed (multimodal therapy).
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Alternatively, effective analgesia may require the

use of sophisticated techniques, such as patient
controlled analgesia (PCA) or epidural infusion
analgesia (EIA). In all surgical procedures there
may be appropriate local anaesthetic nerve/plexus
blocks or simple wound infiltration with local Epidural
anaesthetic drugs used to reduce pain. PCA analgesia
It may be helpful to think of the increasing level
of intervention required with increasing pain in
terms of the WHO analgesic ladder. As a patients
pain intensity escalates, so does the level of Multimodal
support needed (Fig. 14.1, Table 14.2). When therapy
the situation improves and the intensity of the Single-agent
pain decreases, analgesic requirements will also analgesia
decrease and a technique from lower down the
ladder can be used.

Figure 14.1 Analgesic ladder.

TABLE 14.2

PAIN INTENSITY ESCALATION AND MANAGEMENT

Pain intensity Management

Mild Paracetamol or NSAID
Mild-to-moderate Combination analgesic NSAID
Moderate Oral opioid OR combination analgesic NSAID

Moderate-to-severe Oral opioid + paracetamol NSAID

Severe Parenteral opioid (i.v., i.m. or s.c.) + paracetamol NSAID OR epidural
(local anaesthetic opioid)

Combination analgesics are a mixture of weak oral opioid and paracetamol (see next page).

204

PRACTICE POINT
The use of a technique from higher up
the analgesic ladder does not necessarily
mean stopping more simple methods;
epidural analgesia can often be effectively
supplemented by the use of regular
paracetamol or NSAIDs.
Opioids should only be administered by one route
at a time respiratory and other toxic effects
from epidural opioids will be potentiated if oral,
intramuscular or intravenous opioids are given
concurrently. Such toxicity is potentially fatal!
SINGLE AGENT ANALGESIA
Except in minor pain or discomfort, it is unusual
for optimal analgesia to be obtained from a single
agent or technique. If single agent analgesia is
used, it will be more effective if drugs are
prescribed and administered regularly rather than
on an as-required basis. All analgesic drugs can
be given as single agents but are usually more
effective when given as part of a balanced
multimodal therapy regimen.
MULTIMODAL THERAPY
It is often difficult to produce safe, effective
analgesia with a single group of drugs. Better
results with fewer side effects are achieved if
combinations of drugs affecting different parts
of the pain pathway are used. Such balanced
analgesia (multimodal therapy) usually consists
of a combination of local anaesthetics, opioids
and NSAIDs, and paracetamol.
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CHAPTER 14 | PAIN MANAGEMENT
ANALGESIC AGENTS
Paracetamol
This is a very useful drug that has a high
therapeutic index and very few side effects in
normal dosage. It is toxic in overdose because it
depletes the glutathione reserve of the liver and
then damages hepatocytes. Paracetamol should
be given regularly and can be administered by
oral, rectal or, more recently, the intravenous
route (as the pro-drug pro-paracetamol). It should
form the basis of most in-hospital pain regimens.
Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs are increasingly used as part of balanced
analgesia as adjuncts to opioid analgesia in an
attempt to increase efficacy and reduce opioid
side effects. Different preparations are available
for dosing by sublingual, oral, rectal and parenteral
routes. This group of drugs is unlikely to be
chosen for the management of pain relief in the
critically ill patient due to effects on haemostasis
and renal function.
PRACTICE POINT
NSAIDs are often contra-indicated in critically
ill patients due to their potentially disastrous
effects on renal function and gastric mucosa.
NSAIDs are absolutely contra-indicated in the
elderly hypotensive patient.
The COX-2 inhibitors are a newer subgroup;
however, they are substantially more expensive
than standard NSAIDs and accumulating evidence
suggests that gastrointestinal side effects may
not be substantially different and efficacy is no
greater. They should not be used in patients with
ischaemic heart disease.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
Opioids
Codeine phosphate is an opioid with weak analgesic
properties and, in randomised controlled trials,
has an efficacy equal to paracetamol in adequate
dose. However, it is profoundly constipating and
may produce substantial nausea which limits its
usefulness. It is often used in combination
preparations with paracetamol.
Tramadol is a stronger opioid than codeine. It has
many opioid-like properties but without the same
extent of respiratory depression or the tendency
to produce dependence. It does however have a
marked emetic effect in many patients.
Although the bio-availability of morphine is quite
low by the oral route, adequate effect can easily
be achieved with dose titration. It carries with it
all the usual potential side effects of opioids.
Patients with short-term needs or in transition to
oral medication are best managed with morphine
elixir; for chronic pain, a slow release tablet form
may be most appropriate. Other opioids are also
available orally or as slow release transcutaneous
patches (fentanyl).
Opioids remain the gold standard of analgesia
when a potent agent is required for severe pain.
Morphine is the cheapest and most widely available
agent. The principles discussed apply to all opioids,
as do the toxic effects.
Intravenous opioids bolus doses
Adequate analgesia is most rapidly achieved by
an intravenous bolus dose, or repeated doses if the
desired effect is not achieved with the initial dose.
Often, boluses of 5 mg are given initially, followed
by further increments of 12 mg until satisfactory
analgesia is achieved. This may require surprisingly
large doses; 2030 mg is commonly needed in an
average sized patient to produce good pain relief.
206
Once analgesia is achieved, i.v. dosing is
commonly maintained by self-administration of
further doses using patient controlled analgesia
(see below).
Intravenous opioid infusions
Although opioid infusions can be very effective,
respiratory and other side effects are common,
and they should only be used in an intensive care
setting. Intravenous opioid infusions are beyond
the scope of the CCrISP course and will not be
considered further.
Intramuscular opioids
The intermittent as-required prescription of
intramuscular opioid analgesia was the traditional
form of postoperative pain relief. However, the
use of 4-hourly intramuscular injections has
repeatedly been shown to be ineffective in a high
proportion of patients recovering from abdominal
surgery and this technique has now been
superceded by more effective methods of analgesia.
It is also painful for the patient and has unreliable
absorption in the hypovolaemic patient.
However a single one-off i.m. dose may allow you
to relieve pain relatively quickly and safely while
organising a more definitive analgesic regimen.
Opioid side effects
The limiting factor for use in the conscious post-
operative patient is the emergence of side effects
in a dose-dependent progression. All opioids
exhibit similar effects, although the profiles of
different agents may differ in the detail.
Respiratory depression
All opioids reduce the sensitivity of the respiratory
centre in the brainstem in a dose-dependent manner.
Even in therapeutic doses, the partial pressure of

carbon dioxide (PaCO2) will show an elevation
from the normal value (5.3 kPa = 40 mmHg).
A high normal (PaCO2) of up to 6.5 kPa should
be considered an expected consequence of using
such drugs (as should constricted pupils) and is
not a reason to stop using them. Both respiratory
rate and tidal volume are affected by opioids.
Respiratory rate is easier to measure at the
bedside and it is extremely unlikely that dangerous
respiratory depression will occur without a fall
in rate below the normal range (12 breaths/min
in adults).
Sedation
Decreasing level of consciousness carries with it
the risk of loss of protective reflexes, especially
those associated with protection of the airway
(cough, gag and the ability to recognise imminent
regurgitation). As unconsciousness deepens,
airway occlusion may occur.
PRACTICE POINT
A decreased level of consciousness is a
medical emergency if the GCS is less than 8
due to imminent loss of protective reflexes
and ability to maintain the airway.
A low respiratory rate will usually improve
by stopping administration of opioids. If the
respiratory rate falls below 8 breaths/min, if
the patient becomes hypoxic or is at risk from
a decreased level of consciousness, small doses
of the opioid antagonist naloxone may be
indicated (100 mcg repeated until the desired
effect is achieved). Be aware that naloxone may
produce dysphoria, hypertension, tachycardia
and the sudden and unwelcome return of severe
pain if not carefully titrated.
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CHAPTER 14 | PAIN MANAGEMENT
Remember that the half-life for an intravenous
dose of naloxone is short (approximately 1520
minutes) and symptoms may re-appear.
Nausea and vomiting
This is a distressing and common side effect.
It is dose-related and is potentiated by movement
and when gastric emptying is already impaired.
It is caused both by direct stimulation of the
chemoreceptor trigger zone (CTZ) in the medulla
and by gastric distention. Common anti-emetics
available are ondansetron, cyclizine, metoclopramide
and prochlorperazine. Dexamethasone may also
help to relieve nausea.
PRACTICE POINT
Nausea and vomiting may be due to a
surgical cause rather than analgesic regimen
or anaesthesia.
PATIENT CONTROLLED ANALGESIA
The technique is based on the concept of the
patient self-administering a bolus dose of
morphine intravenously (usually 1 mg), after
which the PCA machine will allow no further
demands for a predetermined period the
patient lock-out time. During this lock-out
period, which is usually set at 5 minutes, the
patient is unable to receive further doses. After
the lock-out time has elapsed, the patient is
able to repeat the dose of analgesic drug if they
are still in pain. In this way, the patient titrates
their own level of analgesia, increasing demands
when requirements are high (during physiotherapy
for example) and reducing them when needs
are lower or if they experience side effects.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 14.2

You review a 52-year-old man on the morning of the second postoperative day following a repair
of an incisional hernia which had occurred in an old upper midline scar. Initial assessment shows
the patient to be well built (95 kg), a little drowsy but adequately rousable. His breathing is rapid
(24 breaths/min) and shallow and he cannot breathe deeply enough for you to hear his breath
sounds well. He is sweaty, tachycardic (110 bpm) but normotensive and well perfused. A pulse
oximeter showed SaO2 of 88% initially this has risen to 92% with mask oxygen at 6 l/min. He
has a past history of smoking and mild chronic bronchitis. Review of his charts shows that 4-hourly
morphine 10 mg has been given for analgesia.
You think that he is hypoxic, largely because of poor analgesia.
You increase the flow rate of oxygen to 12 l/min and ask for it to be humidified. The SaO2 increases
to 98%. The patients conscious level improves and he affirms that he is in pain from his wound.
It is 90 min since his last analgesia so you give a further 10 mg i.m. morphine and 20 min later he
is more comfortable auscultation now reveals reasonable air entry but some expiratory wheeze.
Salbutamol (2.5 mg in 5 ml) is given by nebuliser.
Blood gases (on 12 l/min oxygen) show: PaO2 20 kPa (FiO2, 0.6); PaCO2 7 kPa; pH 7.29;
BE 0.4mmol/l; HCO3 28mmol/l.
There is a mild respiratory acidosis and hypercarbia and an acceptable oxygen concentration.
Note that the SaO2 has not told you about the raised PaCO2.
You arrange for review by the on-call physiotherapist and for a chest radiograph. After discussion
with the pain team, arrangements are made for PCA to be established and you prescribe regular
paracetamol 6-hourly either p.o or i.v, and p.o. or p.r. diclofenac 50 mg 8-hourly (having previously
noted that he has normal renal function).
You review the patient at lunchtime. Repeat blood gases 1 h after physiotherapy show marked
improvement. With continuous pulse oximetry, the oxygen flow is steadily reduced to 6 l/min.
The patient is comfortable, breathing well and able to cough at will.

LEARNING POINTS
poor analgesia is common and has profound effects on respiratory and other vital organ
function 4-hourly prn opiates are often inadequate
analgesic techniques are generally better at preventing pain than at rescuing a patient from
marked discomfort with associated complications
review the effect of interventions re-assess your patient!
a multidisciplinary approach can be very useful in pain management.

208

PCA is well accepted by patients and nursing
staff, gaining high levels of patient satisfaction
and providing good quality analgesia. The efficacy
and safety of the technique depends upon the
factors shown in Table 14.3.
TABLE 14.3
CHECK LIST FOR PCA
Does the patient understand PCA? Yes
Do the staff understand PCA? Yes
Is the patient the only person pressing Yes
the button?
Is the pain responsive to opioids? Yes
Is the patient receiving any other No
opioid or sedative drug?
Is the patient receiving a background No
infusion?
Is the patient being monitored Yes
appropriately?
The major advantage of PCA is that it gives the
patient control of their analgesia and greatly
reduces the fear of unrelieved pain. It is also
intrinsically safe; if the patient becomes sedated,
they will administer no further drug, blood levels
will fall, and they will recover consciousness.
Sleep disturbance is a major problem with use
of PCA. The requirement for regular dosing may
prevent the patient having adequate periods of
undisturbed sleep. Often, the pain is severe by the
time the patient re-awakens and takes some time
to bring under control.
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CHAPTER 14 | PAIN MANAGEMENT
PCA is unsuitable for patients who are confused
or who are unable to press the demand button for
physical reasons.
EPIDURAL ANALGESIA (EA)
The most effective way of producing profound
analgesia is to block afferent pain pathways by
the use of epidurally administered local anaesthetic
drugs.
Insertion of the epidural catheter
This procedure is commonly performed by the
anaesthetist at the time of surgery. Both lumbar
and thoracic approaches are used, the latter being
commonly used to provide analgesia for both
thoracic and abdominal surgery.
PRACTICE POINT
Many anaesthetists will not insert an epidural
catheter if the patient has received a dose
of anticoagulant prophylaxis within the last
12 hours. Consult with the anaesthetist if
pre-operative heparin or LMWH are being
considered.
ADMINISTRATION OF EPIDURAL DRUGS
The anaesthetist will have checked the position
of the epidural catheter (ensured that it is in the
epidural space and excluded accidental subdural
or subarachnoid placement) by giving a test dose
of local anaesthetic and will have established an
infusion before the patient leaves the theatre suite.
The infusion will usually be a mixture of a dilute
concentration of local anaesthetic (bupivacaine
0.10.125%) with small amounts of added opioid
(commonly fentanyl 24 mcg/ml). Combinations of
drugs are administered for similar reasons to other
routes better analgesia with fewer side effects.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

CASE SCENARIO 14.3

8 hours after an uncomplicated right total knee replacement, you are asked to review a 59-year-old
woman with ischaemic heart disease who has gradually become hypotensive (BP 80/40) and
tachycardic 110 sinus rhythm.
You assess the patient and find her alert, comfortable and with acceptable perfusion. Continuous
epidural analgesia is in progress, using a mixture of fentanyl and bupivacaine in standard dosage.
There has been no chest pain, dysrhythmia or hypoxia (lowest SaO2 95%). Total volume in the
drains is 750 ml, which the specialist nurse relates as average. The wound is not soaked nor the leg
swollen and the patient has received saline at 150 ml/h since returning from theatre. The epidural
appears to be working well the block is infra-umbilical, the patient can move her toes and is
totally pain free. The infusion is running at 12 ml/h.
You conclude that the patient is hypovolaemic but cannot decide whether postoperative blood loss
or vasodilatation from the epidural is predominant. The patient says she feels thirsty (a good sign
of hypovolaemia). In either event, a fluid challenge is needed and you give 500 ml colloid over 15
min with little effect. During this time, a full blood count shows Hb 11.0 g/dl. You stop the epidural
infusion.
Peripheral perfusion improves but blood pressure fails to respond. There are no signs of on going
bleeding or narcotisation (which can occasionally occur). An ECG shows no acute change. Given
the history of ischaemic heart disease, you are reluctant to give a further 500 ml fluid challenge
so opt for 250 ml over 15 min. The BP begins to rise to 90/50 and the pulse drops to 100. You opt
to give another fluid bolus of 250 ml colloid over 15 min and see the BP rise to 110/60 and pulse
drop to 90. The epidural block is now decreasing and you decide to re-start the infusion at 6 ml/h
and re-assess in 15 min continuing the maintenance fluids.
An hour later, the BP is maintained, there is good urine output indicating adequate renal perfusion
and the patient is comfortable. You make plans to review the patient in 2 h.

LEARNING POINTS
hypotension associated with epidural analgesia is common sympathetic blockade,
peri-operative bleeding and loss of fluid into tissues or through insensible losses can all
contribute and investigations are needed to establish the cause
postoperative bleeding must be actively considered and dealt with
the need for treatment of hypotension due to the epidural alone depends on the level of
the blood pressure, co-morbidity (especially cardiac or peripheral vascular) and the effect
on end organs (urine output)
all patients should be adequately filled with intravenous fluid monitoring by CVP on
HDU may be required in the patient with multiple co-morbidities.

210

The aim is to establish good pain relief with
minimal sympathetic effects and no motor block.
Infusion rates of 815 ml/h are commonly used.
A functioning epidural gives outstanding pain
control.
Troubleshooting epidurals
The two most common problems are breakthrough
pain and hypotension. Both may also be due to
evolving surgical complications. Close co-operation
between the surgical team and the acute pain
service along with clear management protocols
are essential.
Breakthrough pain
This may be due to a problem with the epidural
or the development of a new surgical problem.
The patient should be fully assessed on each
occasion. Help should be sought from the pain
team if it is apparent that the epidural is not
functioning. An increase in the infusion rate
(often preceded by a bolus or top-up dose) may
be required or the catheter may require
re-positioning.
Hypotension
Hypotension is a relatively common problem
with epidural infusions, particularly in younger
patients and in those with higher level blocks.
If hypotension is caused by the epidural, it is
usually due to sympathetic block and consequent
vasodilatation. As there are many other common
causes of hypotension in the postoperative
patient, the epidural must not be assumed to
be responsible until other potential causes have
been excluded. As always, when assessing the
hypotensive patient with an epidural, use the
CCrISP system of assessment to avoid missing
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CHAPTER 14 | PAIN MANAGEMENT
other causes, especially hypovolaemia, bleeding,
myocardial infarction and sepsis (see Case
Scenario 14.3).
Once it has been established that epidural-induced
vasodilatation is the cause of the hypotension,
the infusion should be reduced and adequate fluid
resuscitation should be undertaken to correct the
relative hypovolaemic state.
OTHER LOCAL/REGIONAL TECHNIQUES
There are numerous other techniques based on
the use of local anaesthetic agents, which may be
encountered in specific circumstances. These range
from simple intra-operative infiltration of the
wound to nerve blocks, plexus blocks, intrapleural
infusions and so on. All have their proponents
and specific indications, but all work on the
principle of blocking generation or conduction
of the noxious stimulus to prevent its being
perceived as pain.
PRACTICE POINT
Patients may return to the ward with local
anaesthetic infusions these are severely toxic
if infused intravenously.
This also applies to epidural local anaesthetic
infusions.
CHRONIC PAIN
This is beyond the scope of this text, except to
note that poor management of acute surgical pain
may be one factor in the production of chronic
pain and chronic analgesic dependence.
Paradoxically, the latter is more often produced
by inadequate use of analgesics rather than over
use, as is commonly believed.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

WHERE SHOULD SUCH PATIENTS SUMMARY

BE NURSED? you are an essential member of the acute
pain team, often being the first person called
For many reasons, including the provision of
to a pain related problem
adequate postoperative pain relief, all patients
when assessing the patient in pain, use the
recovering from major surgery should be nursed
CCrISP system of assessment
in an area with a high ratio of nursing staff to
poor pain relief threatens the critically ill patient
patients. Any ward designated for the care of
pain may be due to evolving surgical
patients recovering from major surgery should
complications
have enough trained nurses and doctors to care
pain relief should provide comfort and
for patients requiring PCA or epidural analgesia
restoration of function; analgesia should be
subject to the following provisions:
assessed using reproducible pain scores and
the ability of the patient to cough effectively
1. The establishment of an acute pain service multimodal therapy can dramatically improve
with named consultants responsible for the pain relief and reduce side effects: remember
provision of postoperative pain relief. the concept of the analgesic ladder
PCA and epidural analgesia are very effective
2. Rapid 24-hour availability of designated
techniques but patients need careful monitoring
doctors and resuscitation team.
and regular re-assessment to prevent problems
3. A system for monitoring patients on a regular be in regular contact with the acute pain team
basis including pain scores, respiratory rate or your anaesthetic colleagues!
and sedation scores.
4. Protocols and an education programme for
all staff for the detection and management
of major complications.
5. Availability of continuous monitoring
or transfer to an HDU or ICU for high-risk
cases.

Provision of adequate analgesia is often difficult

and complex in the sick surgical patient:
consideration should be given to transferring
such patients to a higher level of care.

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15
Communication,
organisation
and leadership
in surgical care

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to:
understand the importance of clear
and effective communication in surgical
critical care
appreciate some of the barriers to
communication and ways of overcoming these
develop an increased awareness of the
leadership role, which the surgical registrar
plays in the surgical team
appreciate the value of personal and team
organisation in facilitating this
understand how people normally deal
with adverse events and appreciate the
frequency with which serious traumatic
events can lead to stress reactions.
It is a self-evident fact that being an effective
communicator is a vital skill for all surgeons.
The way care is provided and the expectations
of patients and relatives have changed markedly
in recent times, posing new and challenging
issues for surgical teams. Large numbers of people,
coming from different aspects of the healthcare
professions are now involved in the care of a
single patient and this process needs to be actively
managed by the surgical consultant and his or
her team, who have ultimate and continuing
responsibility for each individual patient. Patients
and relatives, quite rightly, expect good outcomes
from surgical interventions and expect to be kept
informed about details of their care at each stage.
It is vitally important to understand patients
expectations from the outset so that all concerned
can understand what a realistic outcome for that
214
patient may be. It is easy to make assumptions of
what other people think and believe, which often
reflects ones own beliefs rather than the reality
for that individual. Many problems arising in
surgical care are the result of poor communication,
often serial, rather than a lack of knowledge or
an incorrect decision. There is evidence to suggest
that adverse outcomes, iatrogenic injuries, failure
to provide adequate care, mistakes, providing
incorrect care or system errors are more likely
to lead to litigation or complaints if there have
been preceding communication problems. Other
international data on litigation have shown
adverse outcomes occurring in 3.7% of admissions
with 1 in 4 (1% of total) due to negligence.
However, two out of three claims come from
patients with no adverse outcome or an adverse
outcome not due to negligence. Another study
has shown that only 3% of patients who suffered
negligence filed a lawsuit. Reasons given for
instigating litigation include a desire to correct
apparent deficient standards of care, to find out
what happened and why, to enforce accountability
and to gain compensation for accrued and future
costs. A further study has shown that 70% of
litigation is related to poor communication, citing
feelings such as desertion, devaluation, lack of
information and lack of understanding. In one
study, over half of patients who commenced
litigation claimed that they were so unimpressed
by the doctor that they wanted to sue him/her
before the alleged event occurred.
For the surgical team to function at its best, and
thereby stand any chance of delivering optimum
levels of care consistently, there must be good
communication, organisation and leadership within
the immediate team and with others. To achieve
this, you need to understand some aspects of the
ways in which people function under these
 CHAPTER 15 | COMMUNICATION, ORGANISATION AND LEADERSHIP IN SURGICAL CARE

circumstances, to learn to communicate better avoidance of leading and multiple questions;

and to think about the ways in which you can knowledge of and methods to overcome responses
contribute to the overall functioning and well-being such as denial and blocking; understanding and
of your team. Consider, for a moment, the range use of empathic statements (see glossary).
of tasks and scenarios you might face as a busy
surgical registrar on call over a weekend, where
TABLE 15.1
communication, leadership and team skills are
essential to a successful outcome. Having COMMUNICATION SKILLS AND
considered these skills, refer to Table 15.1 for
ORGANISATIONAL ISSUES TYPICALLY
a list of examples.
USED OR ENCOUNTERED DURING A
WEEKEND ON CALL
COMMUNICATION Some tasks/processes
Communication matters not just with the Informing patients and relatives of their
patient and relatives but also with colleagues. condition and progress
It is important to be able to communicate Obtaining consent for interventions
effectively for many reasons: Breaking bad news to patients or relatives
to elicit and to provide information quickly Arranging investigations and ensuring
and accurately. Especially in the critical care the results are seen and acted upon
setting, the quality and efficiency of this Conducting ward rounds
aspect of communication (data transmission) Speaking to senior colleagues
is important Speaking to junior colleagues
to be able to respond to psychological and Booking cases for operating theatre and
emotional issues in colleagues, patients and ICU/HDU
relatives (empathy, understanding and emotional Coping with multiple jobs
support). This may contribute to improved Speaking to multiprofessional team members
outcome and will improve satisfaction ratings Dealing with emergencies
and reduce complaints Delegation and seeking help
to be aware of the possibility of tension or Identifying and treating patients
distress building up within the team and to know in clinical priority
how to respond to this. Your team will not Some skills
work well when it carries this type of burden. Planning Leadership
A comprehensive account of basic communication Active listening Mirroring
skills is outside the remit of this chapter, although Empathy Checking back
certain relevant communication skills are discussed Assertiveness Summarising
and practised on the CCrISP course. You should Use of silent pauses Prioritisation
develop an awareness of basic communication Time management Delegation
skills including: the appropriate use of open, Avoiding aggressiveness
focused and closed questions; knowledge and

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
WHAT ARE THE SPECIFIC
COMMUNICATION PROBLEMS?
Often, surgical critical care takes place in an
environment where background obstacles to
communication are more likely. The patients are
ill and frightened, and the staff are often over-
busy. The patient may be unable to concentrate,
especially if there is pain, severe illness or
complications of medication. Equally, operational
fatigue on the part of staff is also important.
It is often easier for others to recognise the
signs than for individuals to identify themselves.
Signs of operational fatigue include loss of clinical
sharpness and reduction in the quality of decision-
making. Other obstacles to communication may
include irritability and anger, high tension,
confusion (most obvious in organic brain
syndromes but may also occur in functional
disorders), distress and tearfulness, and high
expectations from patients and relatives but also
from self and colleagues.
SPECIFIC COMMUNICATIONS STRATEGIES
The critical care setting
Strategies need to be targeted at the difficulties
likely to be experienced. Critical care settings
can be bewildering for patients and their relatives
often with a lot of unfamiliar equipment, sometimes
with limited access to natural light. It is easy to
assume that patients, relatives and doctors have
a greater knowledge and experience of these
environments than they actually have. It is
especially important that at each stage, explanations
are provided. These can be very simple tasks,
such as explaining the role of a particular piece
of equipment, an account of the next intervention
or an explanation of where a specific issue fits
216
into the overall management plan. It can be
helpful to try to predict what may happen and
have a plan for the different possibilities. With
regard to patients, especially the elderly, if they
are in an environment with limited natural light,
this may increase disorientation. Readable clocks
or other ways of helping to overcome this are
important. Especially where there is a degree of
organic confusion, aids to orientation can be
important, such as photographs of loved ones,
and easy-to-read name badges.
It may be necessary to repeat both questions
and explanations at different times. Being prepared
to go back over the history after the immediate
crisis is good clinical practice and may reveal
issues previously unconsidered. It should be
realised that many communication situations
are not single episodes but rather a continuous
process involving multiple episodes over time.
Similarly, it is helpful to reduce fear by offering
repeated explanations and using check-backs to
assess that patient and relatives have understood.
Patients can often only recall only small amounts
of the information provided from a single
communication episode.
Breaking bad news
There is no perfect way to set out any
communication process what works well with
some people in some situations can fail in others.
However, some general principles are probably
helpful. It can be useful to think about this is terms
of what educators call the set. This includes the
environment where the communication episode
will take place and who will be present. It also
includes an introduction as to the purpose of the
episode, the details of the episode itself and then
a summary of the salient points of the discussion.
 CHAPTER 15 | COMMUNICATION, ORGANISATION AND LEADERSHIP IN SURGICAL CARE
When speaking to relatives, it is important to
ascertain that the patient has given permission
for relatives to be informed of their condition.
Understanding, if possible, intra-family dynamics
can also help manage communications with
relatives. For example, in some circumstances
it may be felt necessary for the medical staff to
talk to several family members together, while
in others a family spokesperson may be the best
person to communicate with.
In terms of breaking bad news, an important
principle is to be prepared to talk, and listen.
The barriers to doing this may come from
patients (or relatives if they are receiving the
communication) or directly from us. Some things
are hard for us to talk about but, in this setting,
it is important to be able to tackle these. One way
of starting such a conversation is to ask an open
question such as what is your understanding of
the present situation?, or what have you been
told so far?. In this way, you are giving the
patient or relative the first opportunity to have
a say and it may help you understand their
expectations and how much they wish to be told.
Some patients want a lot of detail, others only a
broad outline. If you are unaware of the patients
expectations at the outset, you will not be able to
meet them and you should not make assumptions.
Starting in this way also gives you the opportunity
to show that you are listening and to pick up on
any verbal or physical clues as to the patients
or relatives underlying emotions. These can be
subtle and you need to consciously look for
them. You need to be prepared to use direct and
understandable language. It is a great temptation
to beat around the bush in an attempt to soften
the blow but it is important to say difficult,
emotive words such as cancer or death, should news has made you feel more fearful than anything
they be appropriate. It is often uncertainty that
people find difficult to handle; once they know
what they are facing, they can start to deal with
it and patients will often thank you for being
frank and honest. Clearly, however, this can still
be a delicate situation.
Attitudes have changed substantially in the last
two decades but the work of John Hinton in the
1970s with people who had terminal illnesses
remains instructive. He found that, in an in-patient
unit, though staff believed that only a small
minority of patients knew of their diagnosis and
prognosis, a substantial majority had a very good
understanding. This knowledge was acquired in
various ways, including overhearing bedside
conversations or reading case files. They were
able and willing to share this with Hinton in a
way that they had not done with the other staff.
Importantly, when asked why they did not discuss
their knowledge with staff, patients often indicated
that they did not want to cause the staff distress.
In other words, patients chose silence partly to
protect the staff working with them. From this,
the concept arose of being prepared and able to
give the patient permission to talk about bad news.
To be able to give permission effectively requires
good listening skills. Listening is an active
process, interspersed with signs of encouragement.
We all do this differently but should use attitude,
facial expression or verbal acknowledgements to
show interest and encourage further disclosure.
The use of empathic statements can be a straight-
forward way of identifying feelings and indicating
support. These are statements in which the
interviewer tries to identify a current feeling such
as sadness, anger or fear and then ties it to what
has been happening, such as It sounds as if this
else. This can allow the person to talk about
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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
feelings and it also gives the interviewer a chance
to check if what he/she perceives is correct. There
are different ways of responding to sadness, anger
and fear, for example. In contrast, sympathetic
statements such as I know just how you feel,
should be avoided. It is very unlikely that you
could feel the same and such statements can lead
to aggressive reactions from patients or relatives.
The most important aspects of helping people talk
about feelings are to allow time and space. The
setting should be quiet and private. The interviewer
should give a sense of having time to talk. Often
it will not take much time (in general, more skilled
communicators take less time than less skilled
communicators) but it does require planning to
ensure, for example, that discussions like this are
not started a few seconds before a ward round or
some other fixed event. There is evidence to show
that if a person is left to talk freely that they will
speak for between 4080 seconds. Allowing them
to do so will start things off on the right footing
and help the patient think you care about their
problem. Sitting down to talk to the patient is
good not only from the body language point of
view but gives the impression of more time being
taken. In a study where a doctor, who was either
sitting or standing, spoke to patients for a set
length of time, the patients estimation of how
long the doctor had spent with them was doubled
if the doctor had sat down.
Another aspect of communication to be aware
of is the use of mirroring. The doctor mirrors
what the patient is doing in terms of their tone
and speed of speech, and their body language.
For example, if a patient is sounding timid and
scared, using a similar tone may convince the
patient that they are being listened to and dealt
with appropriately. If they are leaning forward,
218
you should lean forward. It is not suggested that
everything a patient does should be mirrored but
doing the opposite to what the patient is doing
can send a message that you are not listening or
concerned about them.
A further issue for more junior doctors in particular
is the way they handle their own uncertainties.
In general, patients want definite statements and
guarantees of outcomes. Clearly, there is much
uncertainty surrounding surgical outcomes and
you need to be able to appear confident in your
knowledge, yet not lead patients to have unrealistic
expectations.
At the end of the discussion, it is useful to make
it clear that further meetings can be arranged and
to give details of how this can be done. Giving
the family a liaison person can often provide
reassurance that it should be easy to talk again.
It is also important to document in the patients
notes that he or she has been spoken to, to provide
a brief outline of what was said and to record any
issues that may be relevant in the future.
Medical mistakes
Occasionally, people come to harm following
a medical complication or a medical error. This
raises quite different communication issues.
In addition to breaking bad news, there is the
additional matter of handling guilt feelings and
fear of litigation. Again, it is not possible to make
absolute statements but, in general, even in these
situations, it is important to explain as fully as
possible and, if an error has been made, to offer
an apology. Not only is this in keeping with
current thinking in the NHS but, since a sense of
injustice often drives litigation, it is probably also
a part of good risk management. It is important
to be clear that one cannot apologise for the
actions of others you can state that you are
 CHAPTER 15 | COMMUNICATION, ORGANISATION AND LEADERSHIP IN SURGICAL CARE
sorry to hear of their concerns/worries and that
they are entitled to a full reply to questions/
complaints. It is dangerous to apologise for an
event that occurs outwith the individual doctors
control (i.e. by another doctor or member of staff).
It is also important to realise that you should
not criticise actions of others without very careful
consideration. The GMC Good Doctor Guidelines
stresses the importance of collegiality and it is
very easy to comment on something without
knowing the full details. Criticism of others is
easy to imply by the most innocent off-hand
remarks or ill-guarded body language. In certain
cases, such actions can give the patient the
justification in their mind to make a complaint
or to seek legal advice.
Working with colleagues
Staff relationships are of particular importance
in critical care settings. Not only does the work
involve vulnerable and dependent patients, it also
carries with it a lot of work-related emotional
issues. It is easy for these pressures to translate
into aggression and lack of respect. They may be
made worse when inter-professional rivalries
intervene or when people normally outside the
unit are involved with particular patients.
Ideally, there needs to be some way for these
issues to be dealt with on a team basis identifying
problem areas and finding supportive and
effective ways of achieving change. Methods of
achieving this cannot be prescribed but must vary
with the precise situation. Deficient communication
must be addressed, whether within or between
professional groups, either by individual or group
meetings, and formally or informally. These
techniques often remain alien to the medical
profession but can help greatly in the development
of efficient and good-humoured units. Individuals
219
should also show respect in their own behaviour
and learn how to use assertive rather than
aggressive or passive interaction (see glossary).
EVERYDAY COMMUNICATION IN
SURGICAL CARE: ORGANISATIONAL
SKILLS
Surgical training covers basic knowledge, operative
skills and, through courses such as the CCrISP
course, guidance in practical management of
acute conditions. Only infrequently do trainees
receive advice or instruction about the organisation
of their practice. Regrettably, this is often discovered
through trial and error.
In any training programme, there is a point
where the surgical trainee begins to take increased
responsibility for hour-to-hour management of
patients, for critical decision-making about the
requirements for treatment of emergencies, and
to carry out major and emergency operations as
appropriate. This has historically been on promotion
to the registrar grade in the UK. Nowadays, the
stage at which this occurs will vary but there is
always a sizeable step-up in responsibility at some
point in surgical training. Ultimate responsibility
rests with the consultant in charge but no surgeon
can expect to carry out procedures without sharing
responsibility for peri-operative care.
Therefore, the senior trainee will often be
responsible for the daily business ward rounds,
reporting as necessary to the consultant. It is
unlikely that the consultant will make a formal
ward round every day so it is essential that the
trainee actively manages the patients, looks for
and identifies problems, makes decisions about
management and contacts the consultant when
appropriate. Initially, the trainee will communicate
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
very frequently with his senior but, with training
and experience, the scope for safe practice can
and should expand.
For care to be delivered successfully in the context
of a busy surgical practice, there are many facets
of care during the working day including decision-
making, investigations and operations. These do
not happen automatically! As the trainee, you
have to learn to conduct this orchestra of activity,
and it is not always an easy task. To achieve
success, you will need to organise yourself (and
sometimes others), exercise a degree of leadership,
communicate effectively and be able to make
appropriate decisions.
To make decisions, you need information and
you get this from communication. As you train,
you need to become aware of what information
you do need and what information is largely
superfluous to any critical decision. There is a
balance to be struck between hasty and unfounded
decision-making and un-necessary delay waiting
for tests that will add little or nothing. Getting
information takes you or others time and you
need to delegate and organise appropriately.
To be efficient, you need to time-table your
business ward rounds such that key information
is most likely to be readily available from nurses
and house staff. You need to be prepared to
circumvent blocks to your patients progress.
It may prove difficult to get old notes, get a
certain test or opinion, administer a certain drug.
At times you will need to be quite assertive on
your patients behalf to get what they need but
you need to learn when to be, and when not to
be, assertive. Building up good personal working
relationships between other key members of staff
will often help in this regard. The ward sister,
the out-reach nurse, a clinical nurse specialist, the
220
emergency theatre sister and a friendly radiologist
are just some examples. Think about the people
who can make things happen for your patient and
for you.
ORGANISE TO MAKE COMMUNICATION
EASY AND RAPID
To get the best out of a team, leadership is
required this requires a range of skills including
ability, knowledge, personability, decision-making,
appropriate humour, humility, acceptance of other
views and firmness. All must be deployed at the
right time and few, if any of us, possess all or
even a majority of these attributes. You will need
to work hard, praise and support your colleagues,
admit when you are wrong or do not know and
get timely help. Dealing with seniors is a whole
skill in itself. Few consultants will not wish to
be informed promptly about unwell patients but
all will expect you to have assessed the patient,
begun immediate treatment and arrived at some
decisions including a provisional plan of action.
The exception to this is the patient who clearly
needs an immediate operation beyond your
ability for example, a collapsed patient with
penetrating trauma where the consultant will
want a brief clear message and probably give
you a brief and clear reply!
Clinically, you will need to lead by example
if you are not thorough, why will anyone else be?
Re-assessing patients is probably the single most
neglected skill clinical patterns will emerge and
diagnoses become obvious. With current working
practices this is becoming more difficult and
greater organisation is required for achievement.
This underpins one of the basic CCrISP principles,
of re-assessment after making decisions or
instigating interventions. Utilise the support
 CHAPTER 15 | COMMUNICATION, ORGANISATION AND LEADERSHIP IN SURGICAL CARE
services available good and experienced nurses
can give you an enormous amount, particularly
about how unwell a patient is.
Managing emergencies and deciding on the
need for urgent surgery is difficult. Patients need
a diagnosis and unstable patients need treatment
urgently. Regrettably, patients do not magically
improve between 2 a.m. and the 8 a.m. ward
round the emergency patient who fails to
respond to simple resuscitation in the middle
of the night needs a plan of action made then.
This may involve conservative or operative
treatment but lack of knowledge or an inability
to conduct a particular operation is never an
adequate reason for delay. Decision-making is
active not passive!
Continuity of care is essential for patient well-
being in critical illness. Junior doctor hours have
changed but the need has not the onus is now
on the owning team to pass on problems to the
duty team, but also on the duty team to look for
problems among the patients of all the surgical
teams and to deal with them promptly. This poses
the challenging communication task of a surgical
handover when the responsibility of a large
number of patients needs to be passed on to a
different team. Within this patient group there
will be patients who need specific interventions
in a timely manner, patients who are getting better
and do not need anything specific, patients who
are at high risk of having problems, those who
have not yet been fully sorted out and those who
deteriorate unexpectedly. This latter group should
be very small if the CCrISP principles of pro-active
management, particularly for those who are
slow or fail to progress, are adhered to. A written
handover list with a concise summary of each
patient and a categorisation into one of the above
categories is invaluable in this situation. This
should be supplemented by a verbal reinforcement
of which patients are giving cause for concern
and some acknowledgement from the doctor
receiving the handover that these patients have
been identified and the responsibility accepted.
Assuming the incoming doctor will pick up on
these things instinctively is not acceptable.
Progressing up the surgical training ladder is a
stressful but enormously rewarding time. You will
very quickly develop new operative and patient
management skills and begin to feel that you
really are a surgeon. Organise yourself and your
practice and communicate and listen effectively
to make the learning process less stressful for all.
COPING WITH ADVERSE EVENTS
Emotionally charged events are common in
everyday life and particularly so in the critical
care setting. This holds true for relatives and
staff as well as for patients. Coming to terms
with these everyday events is a largely automatic
process. In simple terms, it seems to include
having an awareness of the emotional reaction
and somehow returning towards a normal balance.
Traumatic stressors are events that produce
intense pressure or tension; they are associated
with the negative emotions of fear and sadness.
In normal circumstances, these emotional
reactions gradually decline and each subsequent
recall of these feelings is rather less intense until
eventually, as a new equilibrium is reached,
the emotional reaction fades completely and the
individual adapts.
Faced with events that are perceived to be
especially traumatic, this adaptive mechanism
may be overwhelmed. The initial emotional
reaction may be so intense that the only viable
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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
reaction is to attempt to prevent or avoid (blot
out) these painful feelings. This may be achieved
by avoiding places or objects that remind the
person about the trauma, or through suppression
of emotions in general emotional numbing.
These defensive reactions will rarely be completely
successful and the individual is left with painful
intrusive recollections, which alternate with
defensive avoidance. This cyclical reaction of
intrusion and avoidance is the central element of
post traumatic stress disorder (PTSD). It is possible
that, as the emotions are suppressed because they
are too extreme, they are not held in awareness
and do not decline. The condition becomes chronic
and may be frankly disabling. Stress disorders are
not rare: some symptoms of PTSD are seen in the
majority of patients who are involved in significant
accidents and features occur in relatives of the
victims and staff. Typically, patients may report
recurrent and intrusive distressing recollections
of the event including flashback episodes. These
can be precipitated by cues, which symbolise or
resemble an aspect of the traumatic event (e.g.
hearing a cars brakes on TV or even driving
past the hospital). The victim is likely to avoid
thoughts or cues that activate memories of the
event and may become withdrawn, detached or
appear depressed.
Critical events are a significant cause of
occupational stress for staff groups (including
doctors) in this environment and this is important
to recognise not only for personal and team
well-being but also because operational fatigue
and impaired performance may result. Awareness
of stress reactions is the first step and the provision
of appropriate support of colleagues and patients,
largely through opportunities for discussion, will
represent a significant advance in many settings.
The initial aim is to provide a means for people
222
to talk about a critical event, learning about some
of the ways that people may respond and
(usually) achieving an understanding that their
own behaviour is within a normal range.
COMMON PSYCHOLOGICAL DISORDERS
IN SURGICAL CRITICAL CARE
So far, the emphasis has been on specific reactions
to adversity but of course a wide range of problems
may occur. Traumatic life events may trigger
feelings of depression, anxiety or even relapse of
certain psychoses. The assessment needs to cover
the full range of psychological difficulties. In this
section, brief reference will be made to four
of these.
ANXIETY
Mild feelings of fear, apprehension, sadness and
emotional turmoil are very common in anyone
admitted to hospital with a serious condition.
In general, the approach taken by the clinical
team can often determine the amount of distress
experienced. A team that works well together,
communicates well with patients and offers
appropriate emotional support will reduce these
difficulties, while dysfunctional teams will
exacerbate the problem.
Assessment is likely to centre on asking appropriate
questions about current feelings and enquiring
into any associated autonomic symptoms of
anxiety (e.g. tachycardia, raised blood pressure)
which may mislead in the assessment of physical
health. Sometimes, visible over-breathing
(excessive, often irregular breathing) may be a
clue to the presence of the chronic hyperventilation
syndrome. This can present with a multitude of
physical symptoms and is often associated with
anxiety or depression.
 CHAPTER 15 | COMMUNICATION, ORGANISATION AND LEADERSHIP IN SURGICAL CARE
Major depression
Depression is also a common condition and often
unrecognised. It spans a wide range of severities
and patterns of reaction. The core feature is a
depressed mood, in which there is loss of pleasure
and enjoyment, reduced interest, hopelessness and
helplessness, and pessimism for the future. In
addition, there are often biological features, such
as loss of weight, impaired sleep with early morning
wakening and a diurnal variation of mood
worst in the early morning. Finally, there may be
evidence of a frank psychosis with mood-congruent
delusions and hallucinations. These may include
delusions of worthlessness or guilt, delusions of
cancer, delusions of persecution (felt to be deserved),
accusatory auditory hallucination. All these are
in keeping with the primary disturbance of mood.
As a routine in the assessment of psychiatric
disturbance, there should be an investigation of
suicidal thinking. One of the ways of asking about
this is to combine a permissions statement with
a question. For example, if someone has talked
about feeling very unhappy, they sometimes can
not see much point in life. Then continue with
something like I wonder if you have ever felt it
would be better just to go to sleep and never wake
up? This can be followed by further questions
about any suicidal thoughts, any suicidal plans
(going into detail if needed) and any suicidal
behaviour. In this way, the whole subject can be
covered easily without causing excessive concern.
There is no excuse for failing to ask about suicidal
thinking in the presence of significant psychiatric
disturbance.
ALCOHOL DEPENDENCE
This is included as a reminder that alcohol
problems are common (in general, about 1 in 5
people in hospital have significant alcohol-related
223
problems) and can cause complications in the
critical care setting. The characteristic problem
arises from withdrawal symptoms, which follow
hospitalisation and enforced abstinence.
These can include typical tremor, nausea, mood
disturbances and confusion but may extend to
delirium tremens and even convulsions.
ACUTE ORGANIC REACTIONS
Variously styled as confusional states, toxic
confusional states, deliriums, etc., these are
short-lived organic disturbances characterised by
confusion, clouding of consciousness (sometimes
quite subtle), disorientation and often marked
fearfulness. There may be delusions often
persecutory. Common causes include alcohol
withdrawal and prescribed medication
(e.g. analgesia) but they may also occur in the
context of a wide range of medical conditions.
Following assessment and correction of the
ABCDs of the initial assessment, further evaluation
is centred on the cognitive state ability to
attend and retrieve, awareness of environment,
etc., and on the possible causes which also require
full assessment. This is an organic disorder in
the psychiatric classification because it is always
secondary to some physical dysfunction. It is
likely to be made worse by a disorientating
environment and by a failure to offer frequent
and repeated explanations.
WHEN TO REFER TO A PSYCHIATRIST?
To some degree, this depends on the capacity
and engagement of the local psychiatric service.
However, there are clear indicators for referral,
which are important to outline. First, there is the
situation where the diagnosis is uncertain and
especially where there may be a psychiatric
component. Somatisation disorder and
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

Munchausens syndrome are extreme examples SUMMARY

but there are often complex interactions between This chapter cannot provide a comprehensive
physical and psychological processes which may account of the field but perhaps it will help to
require assessment. It is important in these highlight those areas where further learning is
situations to make positive psychiatric assessments required. This learning is not readily available
rather than assumptions based on the absence of in text books but can be gained with experience.
signs of physical disorder. It does require insight and reflection on the part
There are situations where either the severity of the individual, the latter skill being easily
of the psychiatric condition or level of danger neglected in a busy surgical environment.
associated with the condition make referral both Communication skills are especially important
appropriate and often urgent. This might be as they help to make practice more effective and
following, for example, deliberate self-harm or efficient. More can be achieved in less time. It is
the development of persecutory beliefs in an acute important to look at patients, relatives and staff
organic reaction leading to thoughts of murder. groups and understand the ways in which we cope
with the everyday workload, with adversity and
One situation in which referral is often considered
how these mechanisms can be overwhelmed at
is in relation to consent. Psychiatrists have special
times of crisis.
knowledge of the legislation to do with consent
to treatment for psychiatric illness. The relevant
legislation has much less to say about consent to
treatment for physical illness and common law
principles usually apply. Nonetheless, as long as a
referral is not made with overoptimistic expectations,
it may still be useful to discuss difficult cases
where consent is withheld as this is an issue
which is more common in psychiatric practice.

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 CHAPTER 15 | COMMUNICATION, ORGANISATION AND LEADERSHIP IN SURGICAL CARE
GLOSSARY
Most clinicians could improve their communication
skills and surgeons are certainly no exception.
The glossary outlines some principles about which
you may wish to read further. The specific skills
cannot be summarised in a short glossary but are
included in most books on communication.
BASIC COMMUNICATION SKILLS
In this section, some of the terminology will be
explained. It is useful in data gathering to use
an appropriate range of open, focused and closed
questions. In taking a history, the open question
Is there anything else? is useful as a final question.
Open questions can take a wide range of
responses, e.g. What is the main problem?
Focused questions can take a limited range of
responses, e.g. Which is the worst pain today?
Closed questions must be answered yes or
no, e.g. Is the pain in the knee the worst
pain that you have?
Some questions are likely to produce misleading
answers. A leading question expects a particular
response and this may be given even if it is
wrong. Multiple questions are common in
checklist approaches to the history but the answer
given may only relate to the final item in the
list again misleading.
225
A leading question expects a particular answer,
e.g. The pain is worst at night, isnt it?
Multiple questions include a list, e.g. Do you
have problems with chest pain, shortness of
breath or ankle swelling? This might attract
the answer no which to the patient might be
no to ankle swelling and to the doctor might
be no to the three items together.
There is a skill to checking back being prepared
to check that you have the right understanding
or using a summary of the main features as a way
of confirming the history with your patient.
There is also a skill to sharing a problem. If you
do not know how to handle something in an
interview, sometimes the best thing is to own up.
For example:
I have a feeling that you are upset but I am
not sure what has caused it. Is it OK to ask you
about it?
My problem is that I only have 5 minutes
before I have to go to theatre. I really need to
ask you about something. Is that alright?
Finally, perhaps the most useful of the active
steps in understanding emotional reactions is the
empathic comment. This is a statement identifying
an emotional reaction, e.g. That must have made
you feel very frightened.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

In making this statement, a lot of care must be
exercised to listen to what is being said and not
simply to assume that everyone will experience
fear, anger, sadness, etc. in specific situations.
It is useful as a way of checking back on emotions
but, more importantly, it communicates that you
can appreciate at least some of what your patient
is feeling. This can be a very powerful intervention
and should be a skill available to all doctors.
ASSERTIVENESS, PASSIVITY AND AGGRESSION
In being assertive, communication allows each
person to express their honest opinions without
needlessly hurting the other person. In being
passive, honest opinions are suppressed.
Aggression involves the use of excessive force
or power causing needless suffering. This can be
active aggression (e.g. violent, insulting speech)
or passive aggression (e.g. emotional manipulation).

Blocking Assertiveness is, therefore, usually the preferred

Not facing an issue. For example, a patient asks
are there any complications with this operation
and the surgeon replies dont you worry, itll all
be fine. Another example is a doctor telling a
patient they have cancer and the patient says it
cant be cancer, I feel too well.
option. In general, assertive statements contain
the pronoun I whereas aggressive statements
more often include the pronoun you, for example,
I feel that the patient would be better helped by
this approach versus You are incompetent
and have got this all wrong.

Mirroring
Reflecting what the patient is saying in terms
of tone of voice and body language. For example,
if a patient is talking softly and timidly, reply
in similar tones. If a patient is sitting leaning
forward, do the same. Doing the opposite
(anti-mirroring) can adversely affect interactions.

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16
Assessment of
surgical risk and
peri-operative care

227
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
OBJECTIVES
This chapter will help you to understand:
the importance of assessing peri-operative risk
the factors that contribute to increased
surgical risk
the peri-operative management of diabetes.
Co-morbidity increases the risk of surgical
procedures and minimising that risk is vitally
important to improve the individual outcome.
Risk assessment is also important in terms of
outcome measures for comparative audit.
Simple scales, such as the American Society
of Anesthesiologists (ASA) grading system, are
open to varied interpretation among experienced
medical assessors, while more complex systems
such as the POSSUM score, are too complex
for most daily clinical applications.
Co-existing diseases can complicate even a simple
operation and increase morbidity and mortality.
The level of care required needs to be anticipated
with consideration given to transfer to units with
appropriate facilities and/or to gaining disease-
directed expertise to advise on pre-operative
optimisation and peri-operative management of
individual co-morbidities.
The concept of a high-risk patient is generally
understood but the key is to recognise the factors
contributing to that perceived risk and repeatedly
(re)assessing these patients throughout their stay
in hospital to minimise the risk of developing
complications.
228
Many of the factors that increase surgical risk are
covered elsewhere in this book. This chapter will
discuss risk assessment in more detail and outline
the specific effects of older age, obesity and, in
particular, diabetes.
CO-MORBIDITIES AND
PERI-OPERATIVE CARE
Good surgical results reflect the quality of care.
This depends on:
surgical factors, relating to pre-, intra- and
postoperative care
patient factors, regarding disease presentation
and pre-existing co-morbidities
systemic factors that relate to the resources
available for the treatment of surgical patients.
Pre-existing co-morbidity increases the risk of
surgery. Anticipation of risk and risk factor
modification are vital in attempting to reduce
surgical morbidity and mortality. Co-morbidities
most commonly associated with increased
surgical morbidity and mortality are:
cardiovascular (hypertension, myocardial
ischaemia, cardiac failure and cardiac
arrhythmias)
chronic respiratory disorders
anaemia
diabetes mellitus
chronic renal impairment
obesity.
Emergency surgical conditions entail higher
risk as do elderly patients because of the higher
incidence of co-existing medical illness and
a reduced physiological reserve.
 CHAPTER 16 | ASSESSMENT OF SURGICAL RISK AND PERI-OPERATIVE CARE
THE METABOLIC RESPONSE TO INJURY
An understanding of the metabolic response to
injury is helpful in understanding how co-morbidity,
particularly diabetes, affects peri-operative
management and risk (see also Chapter 13,
Nutrition). Metabolic responses to major injury,
surgery and severe infection have similar
mechanisms. The response occurs in two phases,
referred to as ebb and flow. The mediators and
their effects for these responses are outlined in
Table 16.1. The ebb phase lasts 2448 hours
and is a neuroendocrine response to tissue injury
and hypovolaemia. Cardiovascular reflex activity
and inhibition of central thermoregulation are
reminders of the fight or flight response. Energy
stores are mobilised to fuel the increased metabolic
demand: plasma glucose concentration increases
in proportion to the severity of the injury due to
mobilisation of liver and skeletal muscle glycogen
stores and the suppression of insulin release that
inhibits the uptake of glucose into cells. Lipolysis
is increased but fatty acid re-esterification within
adipose tissue may be stimulated by the raised
plasma lactate of severe injury or impaired
perfusion of fat deposits. An early rise in hepatic
protein synthesis and an increase in microvascular
permeability are responsible for characteristic
changes in plasma protein concentrations within
6 hours.
Survival beyond the first 12-day initial phase
gives rise to the flow phase of increased metabolic
rate, principally due to muscle catabolism and
resistance to the anabolic effects of insulin.
The triggers for this are similar to the first phase
but with increased energy consumption. The high
energy source ATP is produced principally by
glycolysis (an inefficient mechanism) and the
lactate produced is reconverted into glucose in
229
the liver in an energy-consuming process, thereby
increasing hepatic oxygen consumption and blood
flow. Protein catabolism predominates principally
affecting skeletal muscle but respiratory, gut and
(possibly) cardiac muscle are also affected, giving
rise to problems with mobility, ventilation and
enteral nutrition. There are concomitant increases
in urinary excretion of nitrogen and creatinine.
The increase in proteolysis provides amino acids
as precursors for hepatic gluconeogenesis.
Concentrations of the amino acid glutamine in
skeletal muscle fall. Glutamine is an important
fuel for cells of the immune system and it is a
precursor for glutathione (a free radical scavenger);
it has a role in nitric oxide metabolism and has
also been implicated in the maintenance of the
gut mucosal barrier which may be compromised
after injury. Insulin resistance after injury refers
to its anabolic effects; for example, hepatic glucose
production, lipolysis and the net efflux of amino
acids from skeletal muscle. These effects persist
at plasma glucose and insulin concentrations that
are inhibitory in uninjured subjects. Uptake of
glucose into skeletal muscle is also reduced, an
impairment that involves glucose storage rather
than oxidation. The cause may result partly from
counter-regulatory hormones cortisol, adrenaline
and glucagon, although infusion in healthy
individuals requires much higher plasma
concentrations to cause insulin resistance than
those found in injured or septic patients. So the
effect of these hormones could be augmented
by modulation of insulin sensitivity by
pro-inflammatory cytokines: interleukin-6 in
cancer patients, interleukin-1 in endotoxaemia
and tumour necrosis factor in diabetes and obesity
are all correlated with the degree of insulin
resistance.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
TABLE 16.1
MEDIATORS OF INJURY RESPONSE
AND THEIR EFFECTS
Counter-regulatory hormones
(e.g. catecholamines [adrenaline], cortisol,
glucagon, antidiuretic hormone)
Breakdown of glycogen stores in liver
and skeletal muscle
Suppression of insulin release resulting
in reduced uptake and oxidation of glucose
Increased sympathetic nervous system activity
Lipolysis
Protein metabolism
Increased hepatic synthesis (interleukin-6
induced)
Increased microvascular permeability
Raised plasma concentration of fibrinogen
and C-reactive protein
Fall in plasma albumin concentration
Pro-inflammatory cytokines (e.g. tumour
necrosis factor-, interleukins , 2, 6 and 8
Mimic some responses, but plasma levels
not universally linked to injury indicating
autocrine/paracrine (cf. endocrine) function
Interleukin 6 induction of prostanoids
at the bloodbrain barrier
Activation of the
hypothalamuspituitaryadrenal axis
DIABETES MELLITUS
Diabetes is a state of impaired glucose tolerance
caused either by absolute lack of insulin (type 1)
or relative lack of insulin (type 2). In addition to
the metabolic disturbance, micro- and
macrovascular abnormalities cause retinopathy,
nephropathy, neuropathy, coronary heart disease,
stroke and peripheral vascular disease. Diabetics
also develop cataracts and specific soft tissue
disorders such as diabetic cheiroarthropathy as
a result of exposure of the tissues to
hyperglycaemia, causing accelerated irreversible
biochemical and structural changes normally
found in ageing. Improved glycaemic control in
diabetes protects against these secondary effects.
Surgery can be hazardous to diabetic patients.
The metabolic response to surgical trauma can
rapidly lead to hyperglycaemia and ketoacidosis,
especially in insulin-deficient patients. Poorly
controlled diabetes accelerates catabolism and
delays healing. Insulin and the sulphonylureas
can cause severe hypoglycaemia in fasted and
anorexic patients, which can be particularly
dangerous during general anaesthesia.
Assessment of fitness for surgery, pre-operative
optimisation, an agreed management policy
between specialists and ward staff and meticulous
glycaemic control will greatly reduce the risks of
operating on diabetic patients.
Some case examples will serve to illustrate the
key management issues in patients with diabetes
undergoing surgical treatment.
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 CHAPTER 16 | ASSESSMENT OF SURGICAL RISK AND PERI-OPERATIVE CARE

CASE SCENARIO 16.1

A 33 year-old civil servant, admitted to the surgical unit for an open elective inguinal herniorrhaphy,
is stabilised on thrice daily subcutaneous soluble insulin injection and is otherwise fit and well.
HOW WOULD HIS DIABETES BE MANAGED PERI-OPERATIVELY?
Such patients have absolute deficiency of insulin and require an intravenous glucose-potassium-
insulin (GKI) infusion to be instituted on the morning of surgery after an overnight fast and omission
of the morning insulin dose. A protocol for GKI infusion is given in Table 16.2, though note that
most hospitals will have their own local protocols.
He had an uneventful procedure under general anaesthesia on the morning list with hourly
BM recordings showing good control with plasma levels of glucose between 510 mmol/l. Due to
postoperative nausea and vomiting, the GKI regimen was continued overnight. By the next morning,
he was able to eat and drink normally; the GKI infusion was discontinued and he had his normal
morning insulin dose with his breakfast and was discharged home later that morning.

CASE SCENARIO 16.2

A 67-year old retired coach driver was seen in the pre-admission clinic for work-up for an elective
TURP for symptomatic benign prostatomagaly. He had been diabetic for 5 years and currently
controlled with diet and glibenclamide.
HOW WOULD YOU MANAGE HIS DIABETES?
Generally, type 2 patients well-controlled by diet or oral agents may simply omit their oral agents
and breakfast on the morning of surgery. However, long-acting sulphonylurea drugs (e.g. glibenclamide)
should be substituted by short-acting ones (e.g. glicazide) some days before surgery to reduce the
risk of hypoglycaemia. Blood glucose should be monitored closely in the peri-operative period and
persistent hyperglycaemia should be treated with a GKI infusion. If the patient is in a steady state,
the GKI infusion will maintain satisfactory glycaemic control and prevent hypokalaemia. GKI bags
must be changed if glucose levels are unsatisfactory. Alternatively, insulin may be given as a variable
rate intravenous infusion according to a sliding scale (Table 16.3), which provides greater flexibility.

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CARE OF THE CRITICALLY ILL SURGICAL PATIENT
TABLE 16.2
PROTOCOL FOR GLUCOSE-POTASSIUM-
INSULIN (GKI) INFUSION
For stabilised patients only
For intravenous infusion use 500 ml of 10%
dextrose containing 15 U of soluble insulin
(e.g. Actrapid) and 10 mmol of KCl
infuse at 100 ml/h
check blood glucose every hour
check K+ every 6 h and adjust accordingly
If blood glucose falls to < 5 mmol/l discard
existing bag and replace with 10 U of soluble
insulin and 10 mmol of KCl
If blood glucose rises to > 10 mmol/l discard
existing bag and replace with 20 U of soluble
insulin and 10 mmol/l KCl
Lower or higher insulin doses are sometimes
needed
Check plasma K+ every 6 h and adjust
accordingly
This regimen is only for patients with stable
and well-controlled diabetes; it should be
started on the morning of surgery after an
overnight fast and continued until the patient
can eat and drink normally
232
TABLE 16.3
AN EXAMPLE OF SLIDING SCALE
INSULIN INFUSION
This is for intravenous use in unstable patients
frequently with hyperglycaemia. 50 U of
soluble insulin is added to 50 ml of 0.9%
isotonic saline giving a 1 U/ml solution for
delivery using a syringe driver
hourly monitoring of blood glucose
concentration is mandatory
start infusion at 6 U/h until the glucose
level begins to fall
subsequently, titrate so that blood glucose
falls by 34 mmol/l each hour
most patients need 13 U/h and this
usually becomes clear after 34 hours of
glucose monitoring
A typical sliding scale would be:
blood glucose < 5 mmol/l, give 0.5 ml/h
blood glucose 510 mmol/l, give 2.0 ml/h
blood glucose > 10 mmol/l, give 4.0 ml/h.
 CHAPTER 16 | ASSESSMENT OF SURGICAL RISK AND PERI-OPERATIVE CARE

CASE SCENARIO 16.3

A 66-year-old woman was admitted from A&E with a 6-day history of feeling unwell, with immobility
and discharge from the right foot. She had been diabetic for 7 years treated with diet, glicazide and
metformin. Examination revealed discharge from the instep, a necrotic heel and cellulitis extending
across the ankle into the lower leg. Her pulses were all palpable, but there was diminished pedal
sensation. Her Hb was 11.1 g/dl, white count 18.6 x 109/l, blood glucose 24 mmol/l, potassium 5.8
mmol/l, urea 9.0 mmol/l and creatinine normal.
HOW WOULD YOU MANAGE THIS PATIENT?
She should be managed as per the CCrISP protocol, with immediate attention to the ABCs. Her diabetes
is out of control. An intravenous insulin infusion according to a sliding scale (Table 16.3), with hourly
monitoring of the blood glucose and 34-hourly potassium estimation (Table 16.4) is appropriate.
She requires resuscitation with intravenous 0.9% saline until she has been stabilised, and her glycaemic
and potassium control optimised. Administration of broad-spectrum or best-guess intravenous
antibiotics aid stabilisation of sepsis and the metabolic state prior to definitive treatment of foot
sepsis by debridement or amputation will give the best result. Rarely, gas-forming organisms may
be present; if gas gangrene is suspected, urgent surgery will be required after initial resuscitation.

CASE SCENARIO 16.4

A 68-year-old, overweight woman was admitted in a coma. Her family provided a history of abdominal
pain, anorexia and vomiting for 1 week against a background of 15 years of diabetes mellitus. In the
early years, her diabetes was controlled by diet and oral hypoglycaemic agents; however, for the past
8 years, she had required subcutaneous insulin supplementation. She appeared to be dry and had a
temperature of 38.3C, a pulse of 130/min and systolic blood pressure of 80 mmHg. There was
epigastric fullness and guarding and she had sighing respiration with a smell of acetone on her
breath. A chest X-ray showed basal atalectasis. Blood results showed Hb 10.1 g/dl, WCC 19.5 x 109/l,
Na 152 mmol/l, K 6.7 mmol/l, HCO 15 mmol/l, Cl 100 mmol/l, Ur 22.5 mmol/l, Cr 85mmol/l, glucose
36 mmol/l. Her urine was strongly positive for ketones.
WHAT IS THE MANAGEMENT OF THIS LADY?
Clearly, this is a complex clinical problem that cannot be managed in a general ward. However,
again, the patient should be managed according to the CCrISP protocol with simultaneous immediate
assessment and resuscitation. Although she probably has a surgical problem, she also has diabetic
ketoacidosis (DKA) and this needs to be managed jointly with endocrinologists in an HDU or ICU,
with continuous ECG monitoring and close biochemical monitoring of glucose (hourly) and potassium
(34 hourly) levels (Tables 16.3 and 16.4).

233
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
TABLE 16.4
A POTASSIUM REPLACEMENT REGIMEN
In an unstable patient with varying insulin
requirements, serum potassium levels should
be monitored every 34 hours.
Replacement should be guided by the latest
serum K+ concentration
if K+ > 5.0 mmol/l, omit KCl due to the
risk of cardiac arrhythmias
if K+ 3.55.0 mmol/l, add 20 mmol KCl
to each litre of intravenous fluid
if K+ < 3.5 mmol/l, add 40 mmol KCl to
each litre of intravenous fluid
DKA is uncontrolled hyperglycaemia with
hyperketonaemia severe enough to cause metabolic
acidosis. It is caused by severe insulin deficiency
that stimulates lipolysis and a massive increase
in ketogenesis. It is the hallmark of poorly treated
type 1 diabetes but can occur in type 2 diabetes
when patients are relatively insulin deficient and
there is intercurrent illness stimulating counter
regulatory hormone secretion (especially
glucagon). It carries a mortality of 510% (50%
in elderly patients with DKA precipitated by
myocardial infarction or infection). Prompt diagnosis
and management is essential to prevent death.
As well as hyperglycaemia, hyperketonaemia
occurs due to oxidation of free fatty acids (FFAs)
in hepatocyte mitochondria (a process stimulated
by glucagon and inhibited powerfully by insulin),
yielding ATP and acetyl-CoA. The latter is
converted to acetoacetate, which may be oxidised
to 3-hydroxybutyrate or undergo condensation to
produce acetone. Ketones are transported out of
the liver and used as metabolic fuels by various
234
tissues including the brain; they provide a
few percent of the total energy needs after
an overnight fast but this rises to one-third in
prolonged fasting. When produced in excess,
they accumulate rapidly as uptake mechanisms
become saturated. The main consequences of
raised circulating ketones are:
acidosis, both extracellular and intracellular
diuresis, as osmotically active ketones are
filtered in the urine, exacerbating the osmotic
diuresis caused by glycosuria, and resulting
in polyuria, electrolyte losses, dehydration
and hypovolaemia
nausea by direct stimulation of the
chemoreceptor trigger zone in the medulla.
Simultaneous resuscitation and investigation
includes a 12-lead ECG, bacteriological cultures
of all appropriate fluids including blood and
urine, cardiac enzyme determination and ABG
analysis. Intravenous saline and insulin should
begin immediately (Table 16.3). Urgent treatment
with scrupulous clinical and biochemical
monitoring is essential. Correction of hypovolaemia
will often improve acidosis and hyperglycaemia.
However, over energetic fluid and insulin
replacement can predispose to cerebral oedema
and increase mortality. CVP monitoring for the
elderly and those at risk of heart failure is
required. Monitoring for response is essential.
0.9% saline (with K when appropriate, see Table
16.4) is the fluid of choice. Dextrose 5% is
substituted when plasma glucose has fallen to
1014 mmol/l to prevent hypoglycaemia (insulin
is still required to prevent ketogenesis and
promote glucose utilisation in the tissues).
Use of bicarbonate and hypotonic solutions is
contentious; hypotonic solutions may exacerbate
intracellular movement of water and could lead to
cerebral oedema, while bicarbonate may improve
 CHAPTER 16 | ASSESSMENT OF SURGICAL RISK AND PERI-OPERATIVE CARE

extracellular acidosis; however, as membranes HYPOGLYCAEMIA

are not permeable to HCO3 ions, the all important
intracellular acidosis may not be improved. Indeed,
CO2 can enter the cells to combine with H2O
to produce H2CO3 that can worsen intracellular
acidosis with an adverse impact on outcome.
Hyperosmolar non-ketotic (HONK) state is
distinguished from DKA by the absence of gross
ketonaemia and metabolic acidosis. Hyperglycaemia
may rise to higher levels but insulin levels are
high enough to suppress ketogenesis. It is found
in previously undiagnosed type 2 diabetes and
may be precipitated by intercurrent illness,
diabetogenic drugs (corticosteroids and thiazide
diuretics) or fizzy glucose drinks. Complications
include thrombotic events such as CVA,
peripheral arterial occlusion, DVT and pulmonary
embolism, due to increased blood viscosity.
Mortality exceeds 30% because these patients are
old and often have a serious precipitating illness.
Lactic acidosis is generated rapidly during tissue
anoxia (e.g. shock, cardiac failure or pneumonia)
or when liver gluconeogenesis is impaired.
In diabetes mellitus, it is a rare, but fatal,
complication of biguanides (phenformin, metformin),
which act by inhibiting gluconeogenesis. It presents
as coma with metabolic acidosis and a wide
amino gap due to hyperlactataemia. Blood glucose
levels are usually raised. Treatment is difficult:
intravenous bicarbonate may aggravate intracellular
acidosis; forced ventilation to blow off CO2 may
help; dialysis clears lactate and H+ and will
correct any sodium overload from bicarbonate
infusion. Mortality is high (> 30%) because of
co-existing organ failures.
Hypoglycaemia is a dangerous side-effect of
drugs that raise circulating insulin (i.e. insulin
and sulphonylureas). It does not occur with dietary
restriction, metformin or thiazolidinediones (e.g.
roziglitazone). Common factors that predispose
to hypoglycaemia are outlined in Table 16.5.
TABLE 16.5
COMMON FACTORS CONTRIBUTING
TO HYPOGLYCAEMIA
Accelerated insulin absorption
Exercise
Hot environmental conditions
Unfavourable factors relating to insulin
administration
Too early
Too much
Inadequate food intake
Alcohol consumption
Inhibits hepatic gluconeogenesis
Impaired hypoglycaemic awareness
Diabetes control too tight
Weight loss
Loss of counter-regulatory hormones
Addisons disease
Hypothyroidism
Hypopituitarism
Blunted glucagon secretion (as in
long-standing type 1 diabetes)
Intestinal malabsorption
Renal failure (impaired insulin clearance)

235
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
The events as blood glucose falls are listed in
Table 16.6 but without early recognition can
precipitate a coma. Hypoglycaemia should be
recognised and treated immediately.
PRACTICE POINT
Always remember to check the blood glucose
with a BM stick in any patient with a reduced
level of consciousness.
TABLE 16.6
CLINICAL EVENTS AS BLOOD
GLUCOSE FALLS
~3.8 mmol/l Adrenaline and glucagon
secretion increases
~3.0 mmol/l Onset of hypoglycaemic
symptoms (note, hypoglycaemic
unawareness in some patients)
~2.8 mmol/l Neuroglycopenia and cognitive
impairment
< 1.0 mmol/l Coma
OBESITY
Excessive body weight is an increasing problem
in people of all ages in the UK. The reference scale
for obesity is the BMI, where the BMI is given by
weight (in kg)/height (in m2).
The normal range for BMI is 2025 kg/m2.
Obesity is defined as a greater than 20% increase
over the ideal body weight, which equates to a
BMI over 30 kg/m2.
236
Obesity increases the likelihood of associated
medical disorders including ischaemic heart
disease (especially central obesity), hypertension,
oesophageal reflux, diabetes, obstructive sleep
apnoea, osteoarthrosis, gallstones, varicose veins
and haemorrhoids.
Reaching a diagnosis is often rendered more
difficult. General anaesthesia and surgical
procedures are more hazardous and postoperative
complications, especially those relating to
cardiopulmonary events, venous thrombo-embolism
and the wound, are more frequent.
For elective surgery in non-life threatening
conditions, pre-operative weight loss should be
recommended. For all operations, a minimum
of a blood glucose and ECG should be checked
pre-operatively. Further investigations and
pre-operative optimisation will depend on other
patient and surgical factors. Proceeding to
elective surgery requires a balance of risk versus
benefit and may require careful discussion with
the patient.
ELDERLY
A social definition of elderly includes all those
over 65 years of age and this group comprises
about 1 in 4 patients admitted to surgical wards.
Increasingly, patients over 80 years of age are
being considered for major surgery and these
patients provide a special challenge.
Two main reasons for increased risk with ageing
are the frequent association of age and concurrent
medical problems and decreasing functional
reserve in many organ systems making the
elderly less able to respond to the physiological
consequences of operation. This is especially true
for the respiratory system, cardiovascular system,
 CHAPTER 16 | ASSESSMENT OF SURGICAL RISK AND PERI-OPERATIVE CARE
kidneys, nervous system and drug handling. Again,
careful assessment, optimisation and peri-operative
care should reduce the surgical risk.
RISK ASSESSMENT
Defining levels of risk to patients is important,
both for enhancing the outcome of surgical
intervention, and for managing the expectations
of patients, their relatives and our colleagues.
Verbal and written communication are vital to
the management of expectation in these groups
because there is a general perception that poor
communication by surgeons may hide poor
performance.
Assessment of clinical risk is a complex higher
function to which all doctors aspire and which
forms an integral part of training. Apart from
direct clinical experience, how can we improve
our risk assessment?
Evidence-based medicine provides different levels
of confidence about the outcome of an intervention
when examining published results. The most robust
evidence comes from randomised controlled trials
(RCTs) and meta-analyses of several RCTs on the
same topic, while case-controlled series provide
lower levels of evidence and case reports provide
the lowest (but not always insignificant) form of
evidence. These data often suffer from the constraints
of carefully conducted trials but can be used in
ones own practice to establish criteria for audit.
Audit aims to improve the care of patients by
establishing a standard, identification of areas for
improvement and implementing that improvement,
then evaluating the effects of implementation.
Audit can also be national with contribution of
data to national databases that are being established
by the surgical specialty associations.
237
In the work place, mortality and morbidity
conferences provide a forum in which factors
that have contributed to adverse outcomes can
be debated and strategies may be developed to
improve unit outcomes. National surveys such
as NCEPOD (National Confidential Enquiry into
Patient Outcome and Death) allow panels of experts
to analyse surgical deaths and make conclusions
about their causes and recommendations for
prevention. This can be around pre-operative
preparation, the grade and seniority of staff
involved and the resources available for treatment
(e.g. NCEPOD theatres, ICU and HDU).
Measurement of risk aims to provide some
objective evaluation of individual patient risk and
can allow comparison of individual clinicians or
units. This is fertile soil for research and a recent
Medline search for surgical risk scoring revealed
almost 1500 publications. Thus scoring systems
have been developed in most subspecialties and
for many individual conditions or procedures to
try and produce a scale that will allow an accurate
prediction of outcomes for each patient. Highly
complex scoring systems may be unwieldy in the
clinical situation and, when found to be valid in
one unit or specialty, may require modification
for successful adaptation to other specialties
(e.g. the physiological and operative severity
score for enumeration of mortality and morbidity,
or POSSUM). Simple and more widely applicable
scoring systems such as the ASA grading system
is simple and in wide clinical use (Table 16.7).
Most patients will be assigned an ASA grade
(15) by the anaesthetist assessing the patient pre-
operatively. Although simple and widely used, it is
open to individual variation and even experienced
anaesthetists may vary in their assessment of the
same patient. This blunts its sensitivity and ability
to discern actual risk for each patient.
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

TABLE 16.7

THE ASA SYSTEM FOR GRADING SURGICAL RISK

Grade Definition Mortality (%)

I Normal healthy individual 0.05
II Mild systemic disease, does not limit activity 0.4
III Severe systemic disease, limits activity but is not incapacitating 4.5
IV Incapacitating systemic disease, constantly life-threatening 25
V Moribund, not expected to survive 24 h with or without surgery 50

Risk management is developing in healthcare An international campaign to reduce harm in

and is borrowing ideas and techniques from the
aviation industry that has practised risk avoidance
with great success over many years. In addition
to anticipating risk and the development of
appropriate preventive strategies, a cultural change
around the use of the information is required.
Using adverse incident monitoring as an education
tool, rather than one for apportioning blame,
allows for learning appropriate lessons and putting
strategies in place that minimise the likelihood
of repeated failure. Also, aviation simulators that
reproduce critical incidents allow important skills
to be developed that can then be put into practice
at appropriate moments when real lives are at
stake. In surgery, this translates to the use of
courses like CCrISP and skills laboratories in which
clinical skills and techniques can be practised in
the context of simulated patients and procedures
in order that best practice can be learned and
honed, for use in the clinical arena.
peri-operative care has led to initiatives such as
Patient Safety First within the NHS. This is based
on an acknowledgement by healthcare workers
that events that produce harm in patients are
potentially avoidable. An example of one such
initiative is that of reducing surgical site infections
by establishing a target reduction and examining
compliance with appropriate interventions to
achieve it, including appropriate use of prophylactic
antibiotics, maintaining normothermia, maintaining
glycaemic control in diabetics and using
recommended hair removal methods. In addition,
to increase safety in the operating theatre, the use
of the World Health Organization Surgical Safety
Checklist is being piloted in hospitals. This is a
time-out before surgery (degree of urgency
permitting); at the end of the procedure prior to
transfer to the recovery area, the anaesthetist,
surgeon, scrub nurse and other theatre staff
discuss the patient preparation and any anticipated
critical moments or potential complications and
how these will be managed.

238
 CHAPTER 16 | ASSESSMENT OF SURGICAL RISK AND PERI-OPERATIVE CARE

As champions for risk management, surgeons can

demonstrate leadership in the care of patients that
will improve the outcome of our treatment and
operations.

SUMMARY
it is essential to recognise the factors that
contribute to surgical risk
ensure patients are as fit as possible prior
to surgery
be aware of co-morbidities to predict and
prevent peri-operative problems
manage diabetes carefully and precisely in
the peri-operative period.

239
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

INDEX adenosine 72, 74

adrenal failure 93
ABC approach 26, 35 adrenaline 31, 118, 119
ABCDE 1317 endogenous 229, 230
abdomen -adrenoceptor agonists 118
assessment on ICI 1401 -adrenoceptor agonists 118
burst 148 adult respiratory distress syndrome (ARDS)
compartment syndrome 1423, 1456 49, 177, 178
penetrating trauma 139 adverse events, coping with 2212
re-operative surgery 140, 141, 151 adverse incident monitoring 238
sepsis 151, 171, 175, 176, 178 adverse outcomes
abdominal aortic aneurysm, ruptured 139 communication problems 214
abdominal compartment syndrome 1423, 1456 prevention 3
ABG, see arterial blood gases age
ACE inhibitors 87, 130, 160 and surgical risk 2367
acidbase balance 52, 556, 1034 see also elderly patients
aetiology of disturbances 56 aggressive communication 226
examples of disturbance 578 air bronchogram 41
management of disturbances 56 airway adjuncts 14, 27, 28
acidosis airway management 1314, 267
DKA 2345 escalating need 27
metabolic 55, 56, 57, 58, 104 golden rules 26
respiratory 55, 56, 104 oxygen masks 267, 42
activated protein C 177 techniques 267
acute coronary syndromes 82 tracheostomy 2832
Acute Kidney Injury (AKI) classification 125 see also ventilation
acute organic reactions 223 airway obstruction, episodic 2001
acute renal failure (ARF) 122, 1258 alanine 192
aetiologies 1256 albumin
case scenarios 124, 127, 134 intravenous 189
complications 1323 serum 100, 1945, 230
definition 125 alcohol dependence 223
incidence 125 aldosterone 93, 160
investigations 1289 alkalosis
management 1301 metabolic 56, 58
mortality 122 respiratory 55, 56
patient assessment 128 Allens test 52, 109, 109
prognosis and recovery 133 alteplase (rTPA) 81
acute tubular necrosis (ATN) 126, 129, 133 amino acids 185, 192, 229

240
 INDEX

aminoglycosides 130 arterial line

amiodarone 76 ABG samples 52
anaemia 36 management 108
anaesthetist 14, 27, 98 signal transduction 108
analgesic agents 2057 arterial pressure monitoring 10911
analgesic ladder (WHO) 204, 205 arterial waveform 111
anaphylaxis 93, 100 aseptic techniques 154, 191
anastomotic leakage assertive communication 226
colonic 141, 1501, 172 atelectasis 39, 48
diagnosis 151 atrial fibrillation (AF) 72, 73, 756
risk factors 151 treatment 76
signs of 150 atrial flutter 76
urinary 1656 atropine 79
angina, unstable 82 audit 237
angiotensinaldosterone 157 autonomic manoeuvres 72
anion gap 54 aviation industry 238
anti-diuretic hormone (ADH) 157 AVPU system 17
anti-emetics 207
antibiotics bacteriological samples 99
diarrhoea 189 bag/valve/mask system 27, 28
prophylactic 175, 181 balance salt solution 163, 164
sepsis 173, 175, 177 barotrauma 45, 46
anticoagulation base deficit 54
and epidural analgesia 209 base excess 54
MI 81 -blockers 62, 81, 95, 130
pulmonary embolism 49 beta-2 agonists 37, 38, 132
anuria 128, 145 bicarbonate
definition 123 acidbase balance 55, 56
anxiety, patient 222 infusions 130, 132, 2345
appendicitis 139 normal plasma levels 54
arrhythmias, common causes 74 biguanides 235
arterial blood gases (ABG) 44, 203 bisphosphonate 161
importance in surgical patient 52 bladder pressure, assessment 146
interpretation 534 blood cultures 173
respiratory failure 36 blood gases, see arterial blood gases
samples 52 blood loss
classification 92
see also haemorrhage

241
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

blood pressure 62 C-reactive protein 129

central venous (CVP) 11115 calcium 1601
effect of haemorrhage 95 calcium gluconate 132
elderly patient 62 calcium phosphate 129
non-invasive measurement 107 calcium resonium 133
peripheral arterial 10911 capillary permeability 92, 97
shock 90, 95 capillary refill time 94
septic 96, 97 carbohydrates 185
see also hypertension; hypotension carbon dioxide, partial pressure (PaCO2) 34, 43, 56
blood tests normal range 54
nutritional assessment 1945 pain management 2067, 208
postoperative complications 141 carboxyhaemoglobin 36
renal failure 128, 129 cardiac enzymes 65
blood transfusion 16 cardiac failure 42, 826
body language 218 acute management 86
body mass index (BMI) cardiac filling pressure 95
normal range 236 cardiac index (CI) 96, 119
and nutritional status 184, 194 cardiac output
obesity 236 abdominal compartment syndrome 145
bowel infarction 139 decreased 65, 92, 118, 145
brachial artery cannulation 109 determinants 106
bradyarrhythmias 79 drugs increasing 118, 119
bradycardia 31, 79, 93 measurement 11618
brain, energy demands 1923 in shock 96
brain natriuretic peptide (BNP) 65 cardiac silhouette, enlarged 412
breaking bad news 21618 cardiac tamponade 96
breakthough pain 199, 211 cardiogenic shock 86, 91, 92, 95, 97
breath sounds 64 causes 95
breathing features 95
assessment and treatment 1415 management 97
and pain management 201 cardiovascular disease (CVD) 60
see also respiration; respiratory failure acute coronary syndromes 82
bronchitis 41 atrial fibrillation 756
bronchoalveolar lavage (BAL) 37 atrial flutter 76
bupivacaine 209, 210 bradyarrhythmias 79
burns 92 case scenarios 73, 85
burst abdomen 148 congestive cardiac failure 42, 826
business ward rounds 8, 18, 20, 219, 220 hypertension 87
hypotension 712

242
 INDEX

left bundle branch block 78 shock 93, 101

left ventricular hypertrophy 77 surgical site complications 142, 147, 149
management plan 71 CCrISP assessment system 12, 24
in MOF 177, 179 CCrISP course, aims 3, 9
myocardial infarction 7981 central vein cannulation 11213
right bundle branch block 789 complications 98, 115, 191
right ventricular hypertrophy 778 fluid replacement 114
risks of surgery 867 parenteral nutrition 1901
signs 61 central venous pressure (CVP) 62, 95
tachyarrhythmias 725 abnormalities 17, 63
cardiovascular monitoring and intravascular volume 115
arterial pressure 10911 measurement 98, 99, 11115
blood pressure 107 pitfalls 115
cardiac output/index measurement 11618 sepsis 171
central venous pressure 107, 11115 shock 98, 103
clinical 106 waveform 114
indications 107 cerebral hypoperfusion 61, 94, 99
shock 102, 103 chart review 1819
cardiovascular support 11819 cardiovascular disease 612, 64
cardiovascular system pain management 202
effects of abdominal compartment syndrome respiratory problems 36
145 sepsis 171
examination 645 shock 94
cardioversion 73, 74, 76 see also drug charts; fluid balance charts
carotid sinus massage 72, 74 chest drain 50, 63
case notes 22, 23, 64 chest examination 15
examination 19 chest X-ray
operation records 1389, 144 air bronchogram 41
case scenarios ARDS 177
acid-base disturbance 578 atelectasis 39
cardiovascular disorders 73, 85 bronchitis and emphysema 41
diabetes mellitus 231, 233 cardiovascular disease 42, 656, 84
fluid management 1656 chest drain 50
pain management 199, 208, 210 consolidation 41
patient assessment 19, 22 interpretation 402
prevention of complications 4, 7 Kerley B lines 41, 42
renal failure 124, 127, 134 pericardial effusion 412
respiratory failure 38, 43 pleural effusion 41
sepsis and MOF 172, 174, 1789, 180 renal impairment 128, 133

243
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

respiratory compromise 37, 412 confusion 14, 61, 94

value of 40 conscious level 14, 61, 64
chloride depletion 56 cardiovascular disorders 61, 64
chloride ions 164 causes of alteration 17
chronic obstructive pulmonary disease (COPD) 53 opioid analgesia 202, 207
chronic renal failure 129, 135 respiratory failure 42
clopidogrel 81 shock 94, 96, 99
Clostridium spp. infections 141, 189 consultants
clotting factors, dilution 100 communication with 220
co-morbidity 19, 139 involvement 212, 103
diabetes mellitus 2305 continuity of care 221
and surgical risk 228 continuous positive airway pressure (CPAP) 44
coagulopathy 100, 149, 173 continuum of care 56
Cockcroft Gault formula 135 COPD, see chronic obstructive pulmonary disease
codeine 189, 206 Cori cycle 192
collegiality 219 corrected flow time (FTc) 117
colloid fluids 16, 100 corticosteroids 235
colonic anastomoses, leakage 141, 1501, 172 cortisol 93, 229
colostomy, stoma management 1534 cough, ability 42, 201
communication 21415 CPAP, see continuous positive airway pressure
aggressive vs assertive 226 (CPAP)
bad news 21618 creatine kinase 129
barriers to 216 creatinine
blocking 226 serum 123, 125
body language 218 urine/plasma ratio 130
checking back 225 cricothryoidotomy 14
colleagues/surgical team 21415, 2201 critical care setting 216
liaison person 218 cryoprecipitate 100
medical errors 21819 crystalloid fluids 100
with patients 214, 21619, 2256 CT pulmonary angiography (CTPA) 49
problems arising from poor 214 CURB 65 score 49
questions 216, 225 CVD, see cardiovascular disease
compartment syndrome cyclizine 80
abdominal 1423, 1456 cyclo-oxygenase 2 (COX-2) inhibitors 205
decompression 146, 148 cytokines 168, 194, 229, 230
lower limb 147
complaints 214, 219 daily management plans 201
complementary approaches 2 DC cardioversion 73
complications, see postoperative complications decision making, daily plans 202

244
 INDEX

decision-making 8, 219, 220 EA, see epidural analgesia

definitive care 24 ebb and flow responses 229
delusions 223 ECF, see extracellular fluid
depression, patient 223 echocardiography, trans-thoracic/trans-oesophageal
deterioration, recognition 138, 1401 117
dexamethasone 207 elderly patients
dextrose infusion 234 atrial fibrillation 72
hyperkalaemia 132 blood pressure 62
diabetes mellitus 2305 risks of surgery 2367
DKA 2345 elective surgery 157
HONK 235 electrocardiograph (ECG) 66
hypoglycaemia 2356 atrial tachycardias 756
type 1 231 hyperkalaemia 132
type 2 231, 234 interpretation 6670
diabetic ketoacidosis (DKA) 233, 2345 left bundle branch block 78
dialysis 1301 left ventricular hypertrophy 77
diarrhoea myocardial infarction 7981
enteral feeding 189 normal 701
fluid and electrolytes losses 92, 164 pulmonary embolism 49
diclofenac 208 respiratory failure 367
digoxin 76 right bundle branch block 789
disorientation, patient 216 right ventricular hypertrophy 778
diuretics 86, 133 routine for examining 66
loop 56, 86, 133 shock 98
thiazide 235 supraventricular tachycardia 74
DKA, see diabetic ketoacidosis ventriclar tachyarrhythmias 746
dobutamine 118, 119 electrolytes 65, 15962, 195
dopamine 118 depletion 164
dopexamine 118 see also specific electrolytes
Doppler, trans-oesophageal (TOD) 11617 emergencies, management 7, 8, 9, 156, 221
dorsalis pedis artery, cannulation 109 emotional numbing 2212
drains, management 154 emotions, patients 21718
see also chest drain empathic statements 21718, 2256
drug charts emphysema, chest X-ray 41
cardiovascular assessment 64 endocrine factors, shock 93
pain management 202 endotoxins 185
dyspnoea 61 endotracheal tube 14, 27

245
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

energy fluid balance

assessment of expenditure 194 chronic renal failure 135
requirements 185, 1923 clinical assessment 157
enteral feeding renal failure 134
benefits 1845 and renal perfusion 123, 124
complications 189 fluid balance charts 94, 157, 164, 165
contra-indications 186 fluid challenge 15, 98, 101, 103, 111, 210
routes 1868 fluid compartments 1578
enterostomy, tube 187 fluid management 1516, 1624
epidural analgesia (EA) 200, 204, 20911 biochemical assessment 15862
breakthough pain 211 case scenario 1656
catheter insertion 209 central vein 114
drugs 209, 211 critical illness and emergency surgery 156
hypotension/vasodilation 93, 201, 202, 210, 211 elective surgery 157
troubleshooting 211 epidural analgesia 201
evidence-based medicine 237 renal failure 129
exposure, patient 17 sepsis 1745, 177
extracellular fluid (ECF) 1578 shock 97, 99100
losses 163 fluid overload 157
replacement 164 cardiac failure 834
and sodium balance 159 renal failure 128
extracorporeal life support (ECLS) 47 fluids
colloid 16, 100
failure to progress 7, 8 crystalloid 100
fast-track recovery programmes 157 fresh frozen plasma 100
fasting frusemide 86, 133
chronic renal failure 135 full blood count
metabolic response 1923 ARF 128, 129
fatigue, operational 216 respiratory failure 36
fats, dietary 185 functional residual capacity (FRC) 34
fatty acids 192, 234 fungal infections 173, 180
fear 222
femoral artery cannulation 109 gallop rhythm 95
femoral vein, intravenous feeding 190 gastric emptying 1867
fentanyl 206, 209, 210 gastric residual volume 187, 188
fibrinolytics 81 gastrointestinal fluid, loss 92, 164
fistulae, intestinal 1512, 164, 190

246
 INDEX

gastrostomy HarrisBenedict equation 194

percutaneous endoscopic (PEG) 188 Hartmanns solution 164
stoma management 153 Health Act 2006 Code of Practice 115
tube 187 heart failure, see congestive cardiac failure
glicazide 233 heart rate 62
glomerular filtration rate (GFR) 122, 123 haemorrhagic shock 95
acute renal failure 125 heart rhythm 62
chronic renal failure 135 heart sounds 61, 64, 95
glucagon 193, 229 heparin 49, 81, 209
gluconeogenesis 229 hepatic ischaemia 145
glucose high dependency unit (HDU) 2, 56, 1819
blood levels 229, 2356 high-impact intervention approach 115
as energy source 185 Hinton, John 217
glucosepotassiuminsulin (GKI) infusion 231, 232 history 19
glutamine 192, 193, 229 cardiovascular disease 64
glutathione 229 renal failure 128
glycerol 192 respiratory failure 36
glyceryl trinitrate 80, 133 sepsis 171
glycogen stores 192, 229 HONK, see hyperosmolar non-ketotic state
glycogenolysis 192, 193 hormones
glyconeogenesis 193 counter-regulatory 193, 229, 230, 235
GMC Good Doctor Guidelines 219 shock 93
Guedel airway 14, 27, 28 hospital-acquired infections 48, 154, 1756, 179
hydrogen ion concentration 55, 160, 164
haematuria with casts 128 hypercalcaemia 161
haemodialysis 131 hypercapnia 34, 36, 53
haemofiltration 131 permissive 46
haemoglobin (Hb) 65, 130 hyperchloraemic acidosis 191
haemorrhage 1516, 92 hyperglycaemia 191, 232, 233
classification of blood loss 92 hyperkalaemia 131, 132, 160
coagulopathy 149 ECG changes 132
postoperative 16, 19, 14850 emergency therapy 132
reactive 149 hypermagnesaemia 161
secondary 150 hypermetabolism 194
tracheostomy site 31 hypernatraemia 159
haemorrhagic shock 1516, 91, 92, 95, 101 hyperosmolar non-ketotic (HONK) state 235
hallucinations 223 hypertension 87, 201
hand washing 154 intra-abdominal 145
handover 221 hypertriglyceridaemia 191

247
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

hypocalcaemia 161 inotropic agents 11819

hypoglycaemia 17, 191, 2356 actions 118
clinical events 236 safety 119
factors contributing 235 shock 103, 104
hypokalaemia 56, 70, 160, 166 inspiratory to expiratory (I:E) ratio 46
hypomagnesaemia 161 insulin 192, 193
hyponatraemia 1589 insulin infusion 132, 234
hypophosphataemia 162 sliding scale 232
hypotension 62, 712, 86 insulin resistance 193, 229
epidural analgesia 201, 202, 211 intensive care unit (ICU) 2, 3, 56
sepsis 177 anticipating need 140
hypothermia 99, 100 assessing abdomen 1401
hypotonic solutions 234 discharge 478
hypovolaemia 7, 15, 60, 61, 64 recognising deterioration 140
renal failure 128 shocked patient 103, 104
hypovolaemic shock 91, 92, 95, 101 interleukin-1 194, 229, 168
hypoxaemia 53, 57, 61, 201 interleukin-6 168, 194, 229, 230
hypoxia 26, 107 internal jugular vein, cannulation 113, 190
definition 34 intestinal failure 1956
intestinal fistulae 1512, 164, 190
iatrogenic factors intestinal hypoxia 90, 107
hypovolaemic shock 92 intestinal ischaemia 139, 145
see also medical mistakes intestinal obstruction 190
ileostomy, management 1534 intestines, benefits of enteral nutrition 1845
immunocompromise 1734 intra-abdominal hypertension (IAH) 145
incisions, pain associated 199200 intravascular volume 115, 128
infections intravenous lines, management 63
catheter-related 115, 176, 180, 191 intubation 14, 27, 45
Clostridium spp. 141, 189 investigations
fungal 173, 180 post-operative complications 141
hospital-acquired 48, 154, 176, 179 post-operative pain management 203
hypovolaemia 92 review 20
MRSA 176 targeted 212
respiratory 37 ion exchange resin 133
surgical site 154, 238 iprotropium 37
information, key 220 ischaemic heart disease 7982, 85
inhalers 37 risks of surgery 867
injury, metabolic response 193, 22930 isoprenaline infusion 79

248
 INDEX

jaundice, obstructive 127 local anaesthetics

jejunostomy, tube 187 epidural 209, 210
Joint College Working Party Report on intra-operative infiltration 200, 204, 211
Postoperative Pain 200 loperamide 189
jugular venous pressure (JVP) 62, 84, 95, 96 low molecular weight heparin 49, 81, 209
lung disease, chronic 41, 43, 44, 53
Kerley B lines 41, 42, 84 lung function tests 37
ketone bodies 192 lung protective ventilatory strategy 46
ketones 234
kidneys magnesium 65, 161
functions 122 malnutrition 184, 192
imaging 128, 129 manometer, liquid 113, 114
perfusion 63, 122, 123, 129 mean arterial pressure (MAP) 122
potassium excretion 160 medical mistakes 21819
see also renal failure meningococcal sepsis 93
metabolic acidosis 55, 56, 57, 58, 104
lactate, serum 54, 96, 103, 107, 177 causes 56
language 217 DKA 2345
laparoscopic surgery 200 metabolic alkalosis 56, 58
laparotomy 141, 146, 176 metabolic chart, bedside 194
laryngeal mask airway 27 metabolism
leadership 2201, 239 refractory shock 1034
left bundle branch block 789 response to sepsis 194
left ventricular hypertrophy 77 response to surgery/injury 193, 22930
left ventricular stroke work index (LVSWI) 116 and starvation 1923
limb compartment syndrome 147, 148 metformin 233, 235
line sepsis 191 metoclopramide 80, 207
lipolysis 192, 229 MEWS charts 38
listening skills 217 microbiologist 179
lithium chloride dilution calibration system minerals 185
(LiDCO ) 117 minute volume 45
litigation 214, 219 mirroring 218, 226
liver mitral valve disease 70
dysfunction in TPN 191 mobilisation 198
metabolism 192, 229, 230 MOF, see multiple organ failure
palpation 65 monoclonal antibodies 179
liver function tests (LFT) 129, 173 morphine 80, 206

249
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

mortality nursing staff

national surveys 237 communication with 2201
renal failure 122 HDU/ICU 5
septic shock 168 pain management 2023, 212
MRSA infections 176 tracheostomy management 130
multidisciplinary teams, pain management nutritional prescription 185
200, 208 nutritional status, assessment 1945
multiple organ failure (MOF) 2, 107, 168, 177, nutritional support
179, 181 advanced theory and practice 1924
muscle, skeletal 192, 229 calculating requirements 185
myocardial infarction (MI) 7981 duration 185
acute management 81 enteral
anterior 82 benefits 1845
inferior 81 complications 189
risk of peri-operative 87 contra-indications 186
myocardial ischaemia 201 initiation 1889
myoglobinuria 130 routes 1868
indications 1845
naloxone 207 sepsis 175
National Confidential Enquiry into Patient total parenteral 1901
Outcome and Death (NCEPOD) 237
National Institute for Health and Clinical obesity 236
Excellence (NICE), central venous access 113 obstructive shock 91, 923, 96, 97
National Patient Safety Agency 187 oliguria 96, 123, 124, 145
nausea 207 omeprazole 189
nebulisers 37 ondansetron 207
necrotising fasciitis 150 operation notes 1389, 144
negligence 214 operational fatigue 216
nephrology referral 133 opioids 206
nephrotoxins 1267, 130, 179 antagonist (naloxone) 207
nerve blocks 204, 211 intramuscular 206
neutropenia 141 intravenous 206
nitrates 80, 119 myocardial infarction 80
nociception, defined 198 oral 206
non-steroidal anti-inflammatory drugs (NSAIDs) side effects 201, 2067
204, 205 slow-release 206
noradrenaline 118, 119 toxicity 62, 202, 205

250
 INDEX

organic reactions, acute 223 local anaesthetic nerve/plexus blocks

organisational skills 478, 21920, 221 200, 204, 211
outcomes multidisciplinary team 200, 212
adverse 3, 214 multimodal 205
audit 237 patient assessment 2003
patient expectations 214 patient controlled (PCA) 207, 209
scoring systems 228, 2378 pre-emptive 199
oxygen principles 199200
arterial partial pressure (PaO2 ) 34, 35, 43, 52 reasons for 198
inspired concentration (FiO2 ) 14, 467, 53 and respiration 42, 201, 208
saturation of haemoglobin (SaO2 ) 17, 356, techniques available 2035
52, 133, 208 ward/nursing provision 212
oxygen delivery (DO2) 1067, 116 pain scoring systems 2023
oxygen dissociation curve 34, 35, 52, 53 pancreatitis 187
oxygen therapy paracetamol 204, 205
analgesia 201, 208 passivity 226
failure 43 patient assessment
masks 267, 42 acutely unwell patient 1317
sepsis 175 cardiovascular system 645, 106
shock 97 case scenarios 19, 22
see also ventilation CCrISP system 12, 24
oxygen uptake (VO2) 116 chart review 1819
circulation 1516, 61
pacemakers 87 end of immediate management 17
pain fluid balance 157
breakthrough 199, 211 full 1820
chronic 211 immediate (ABCDE) 1317
definition 198 nutritional status 1945
role of 198 pain management 2003
pain management re-assessment 4, 16, 23, 220
aims of 199 renal failure risk 1267
analgesic agents 2057 stable surgical patient 12, 18
analgesic ladder 204, 205 surgical site 13844
case scenarios 199, 208, 210 unstable patient 212
epidural 200, 204, 20911 patient controlled analgesia (PCA) 207, 209
escalating requirements 199 patient expectations
pain relief 199
surgical outcomes 214
Patient Safety First 238

251
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

percutaneous endoscopic gastrostomy (PEG) replacement in diabetes 234

153, 188 requirement 160
perfusion 62, 90, 1067 potassium chloride 234
peripheral 15, 64, 96 practical skills
renal 122, 123, 124, 129 chest drain insertion 50
pericardial effusion 412 chest X-ray interpretation 402
peripherally inserted central (PICC) line 190 pre-operative assessment
peritoneal lavage 176 nutritional status 1945
pH (arterial blood) 54, 160 renal function 1267
phenformin 235 pressure support ventilation (PSV) 45
phosphate 1612 preventative actions 3
physiotherapy, respiratory 4, 37, 38, 43, 48, 208 case scenarios 4, 7
pink sign 148 renal failure 1267
platelet transfusion 100 respiratory failure 39
pleural effusion 41 sepsis 1767
plexus blocks 204, 211 prochlorperazine 207
pneumonia 489 prognosis, communication with patient 21618
pneumothorax protein catabolism 194, 229, 230
chest drain 50 protein metabolism 229, 230
tension 46, 50, 63, 96, 115 protein-energy malnutrition (PEM) 184, 194
positive end expiratory pressure (PEEP) 456 proteinuria 128
post traumatic stress disorder (PTSD) 222 pseudo-aneurysm formation 52
postoperative complications 138 psychiatric referrals 2234
abdominal compartment syndrome 1456 psychological disorders 2223
anastomotic leakage 141, 1501, 172 psychosis 223
burst abdomen 148 pulmonary angiography, CT (CTPA) 49
case scenarios 142, 147, 149 pulmonary artery catheter
examples and initial presentations 139 (PAC/SwanGanz catheter) 116
haemorrhage 16, 19, 14850 pulmonary embolism 4950, 96
lower limb comparment syndrome 147, 148 pulmonary oedema
necrotising fasciitis 150 cardiogenic 84
warning signs 141 iatrogenic 64
potassium 65, 195 renal failure 128, 133
depletion 164 signs and management 133
low plasma (hypokalaemia) 56, 70, 160, 166 pulmonary secretions, management 3, 4, 37, 38,
raised plasma (hyperkalaemia) 131, 132, 160 43, 48, 208
reducing total body 133 pulmonary sepsis 175
renal excretion 160 pulmonary vascular dysfunction 34
pulse contour cardiac output with indicator

252
 INDEX

dilution (PiCCO) 117 renal failure index 130

pulse oximetry 14, 17, 356, 98 renal function 1223
limitations 36, 201, 203 and acidbase balance 55
mechanism 35 biomarkers 135
pulse pressure 95 renal perfusion 122, 123, 124, 129
pulse rate 62 renal perfusion pressure 122, 123
pulses 15, 61, 62 renal plasma flow (RPF) 122, 123
renal replacement therapy (RRT) 1301
quality of care 228 renal transplant 135
questions 216, 225 reninaldosterone system 160
respiration
radial artery cannulation 52, 109, 110 acidbase balance 55, 57
radiography assessment 1415
renal failure 128, 133 common surgical problems 4850
see also chest X-ray and CVS 61
randomised controlled trials (RCTs) 237 depression in opioid use 2067
RCSS mnemonic 40 and pain management 42, 201, 208
re-assessment 4, 16, 23, 220 respiratory acidosis 55, 56, 104
re-operative surgery 140, 141, 151 causes 56
re-perfusion injury 148 respiratory alkalosis 55, 56
red cell concentrates 99 respiratory failure 15
refeeding syndrome 185, 191 assessment 357
relatives 214, 216 case scenarios 38, 43
renal failure causes 34
aetiologies 1256 clinical signs 35
case scenarios 124, 127, 134 definition 34
chronic 129, 135 discharge from ICU 478
common scenarios in surgical patients 126 management 425
complications 1323 in MOF 177
golden rules 123 prevention 39
intrinsic 129, 130 stable patient plan 378
investigations 1289 ventilation 457
management 12631 respiratory rate 62
in MOF 179 restlessness 96
nephrology referral 133 results, review 20, 65
post-renal 126, 129 rhabdomyolysis 130
pre-renal 129, 130 right bundle branch block 789
prevention 1267 right ventricular failure 114
in severe sepsis 173 right ventricular hypertrophy 778

253
CARE OF THE CRITICALLY ILL SURGICAL PATIENT
risk assessment 2378
see also surgical risk
roziglitazone 235
salbutamol 37, 38, 132, 160
saline, nebulised 42
sedation, opioids 201, 207
Seldinger technique 110, 112
senior colleagues
communication with 220
involvement 212, 103
sepsis
abdominal 171, 175, 176, 178
catheter-related 180, 191
causes 1701
definitions 16970
fungal 173, 180
management 1746
mediators 168, 179
metabolic response to 194
patient assessment 1715
patients at risk 168
prevent, diagnose, act 1767
severe 169, 173
Sepsis Six 176
sepsis syndrome 169, 170, 174
septic shock 90, 91, 93, 94, 169, 177
bacteriological samples 99
clinical features 967
management 100
mortality 168
shock 1516
aetiology 901
blood pressure 90, 95, 97
cardiogenic 86, 92, 95, 97
cardiovascular monitoring/support 1023
case scenarios 93, 101
clinical features 15, 947
continuing assessment 99
254
definition 90
fluid administration 1516, 99100
haemorrhagic/hypovolaemic 1516, 91, 92,
95, 101
ICU transfer 103, 104
inotropic support 103, 104
management principles 97
monitoring and instrumentation 978
neurogenic 93
obstructive 91, 923, 96, 97
patient categories 16
refractory 102, 1034
responses to treatment 100, 102
septic 90, 91, 93, 94, 967, 100, 169, 177
short bowel syndrome 189, 190
simulation, critical incidents 238
sip feeds 186
SIRS, see systemic inflammatory response
syndrome
skeletal muscle 192, 229
skin
examination 65
perfusion 94, 96
smoking 48
SNAP protocol 1512
sodium 15960, 195
basal requirements 159
fractional excretion 130
low serum (hyponatraemia) 15960
raised serum (hypernatraemia) 159
renal excretion 129, 1578
urinary levels 130, 159
sodium bicarbonate infusion 130, 132
sodium nitroprusside 119
sphygmomanometer, automated 107
sputum culture 203
sputum samples 37
stable patient 12, 18
staff relationships 219, 220
 INDEX

Stamm technique 187 systemic inflammatory response syndrome (SIRS)

Starling curve 84, 92, 118, 119 16970
starvation, metabolic response 1923 causes 1701
stoma management 1534 definition 169
streptococci, enteric 175 systemic vascular resistance (SVR) 93, 967, 116
streptokinase 81
stress, in critical care 2, 2212 tachycardia 62, 96, 201
stress response 193 causes 72
stroke index (SI) 116 post-surgical patient 201, 202
stroke volume (SV) 92, 95, 111, 116 sinus 75
sub-optimal care 3 tachypnoea 44, 57, 96
subclavian vein, infraclavicular, cannulation team skills 21415
112, 190 temperature 63
suffering 198 coreperipheral gradient 63, 94, 99
suicidal thinking 223 measurement in shocked patient 99
sulphonylureas 230 postoperative pyrexia 172
super-infections 175 sepsis/SIRS 63
supraventricular tachycardia (SVT), paroxysmal 75 thiazolidinediones 235
surgery, metabolic response 193, 229 thinking on the run 9
surgical handover 221 thyroxine (T4) 193
surgical risk tidal volume (Vt) 45, 46
assessment 2378 tissue perfusion 1067
cardiovascular disease 867 shock 97
diabetes 230 signs of poor 94
elderly patients 2367 tonometry 107
factors increasing 2, 68, 228 total parenteral nutrition (TPN) 1901
and obesity 236 trace metals 162
reduction initiatives 238 tracheostomy 28
surgical site, postoperative assessment 13844 complications 301
surgical team, communication 21415, 2201 indications 28
surgical trainee, role and responsibilities 8, 21920 tube removal 312
Surviving Sepsis Campaign (SSC) 1767 types of tube 289
suxamethonium 160 tramadol 206
SwanGanz catheter 116 trans-oesophageal Doppler (TOD) 11617
sympathetic blockade 93, 201, 211 transducers 1078, 111, 113
sympathetic statements 218 transfusion 100
synchronised intermittent mandatory ventilation trauma
(SIMV) 45 penetrating abdominal 139
syndrome of inappropriate ADH secretion 159 shock 92

255
CARE OF THE CRITICALLY ILL SURGICAL PATIENT

traumatic events 2212 pressure controlled inverse ratio (PCIRV) 467

triglycerides 192 synchronised intermittent mandatory (SIMV) 45
triiodothyronine (T3) 193 weaning 47
troponin levels 65 ventilator-associated pneumonia 48
tumour necrosis factor 168, 229 ventricular ectopics 745
ventricular filling pressure 92
ultrasound ventricular tachycardias 74
abdominal 141 villous atrophy 185, 189
central venous catheter placement 112, 113 visceral perfusion 90, 107
renal 128, 129 vital signs, sepsis 171
unstable patient, management 21, 22 vitamin D 161
uraemia 128, 131 volutrauma 46
urea, urine/plasma ratio 130 vomiting
urinalysis 128 fluid and electrolyte losses 92, 164
urinary anastomoses 1656 opioid analgesia 207
urinary catheter
infection 176, 180 ward
shock management 98 pain management 212
urinary osmolality 130 tracheostomy management 30
urinary retention 7 ward rounds 8, 18, 20, 219, 220
urinary tract obstruction 126, 128 water
urine output 63, 94, 96 abnormal losses 160, 162
acute renal failure 125 basal requirements 158, 162
normal adult 123 oral intake 162
urine specific gravity 130 total body volume 157, 158
urine/plasma osmolality ratio 130 water manometer 113, 114
WaterhouseFriedrichsen syndrome 93
Valsalva manoeuvre 72, 74 wedge pressure 116
vasoconstriction, peripheral 95 weekend on call, communication and organisation
vasodilation 215
epidural analgesia 210, 211 weekend treatment 3, 4
shock 91 weight loss, pre-operative 236
vasodilators 114, 119 wheeze 37
vasopressors 119 white cell count 141, 172, 173
ventilation 457 Witzel technique 187
CPAP 44 World Health Organization (WHO)
lung injury 46 analgesic ladder 204, 205
non-invasive by mask (BIPAP) 45 Surgical Safety Checklist 238
wound management 154

256